Materiały źródłowe

• #1 Pathophysiology of Atherosclerosis

  https://pmc.ncbi.nlm.nih.gov/articles/PMC8954705/

  Atherosclerosis is the main risk factor for cardiovascular disease (CVD), which is the leading cause of mortality worldwide. Atherosclerosis is initiated by endothelium activation and, followed by a cascade of events (accumulation of lipids, fibrous elements, and calcification), triggers the vessel narrowing and activation of inflammatory pathways. The resultant atheroma plaque, along with these processes, results in cardiovascular complications. […] Atherosclerosis initiates upon endothelial dysfunction accompanied by low-density lipoprotein (LDL) retention and its modification in the intima. Modified LDLs, together with additional atherogenic factors, promote the activation of ECs, leading to monocyte recruitment within the intima. Modified LDLs are avidly captured by differentiated monocytes and VSMC, which promote foam cell formation.

• #2 Atherosclerosis – Wikipedia

  https://en.wikipedia.org/wiki/Atherosclerosis

  Atherosclerosis is a pattern of the disease arteriosclerosis, characterized by development of abnormalities called lesions in walls of arteries. This is a chronic inflammatory disease involving many different cell types and is driven by elevated levels of cholesterol in the blood. These lesions may lead to narrowing of the arterial walls due to buildup of atheromatous plaques. […] The exact cause of atherosclerosis is unknown and is proposed to be multifactorial. Risk factors include abnormal cholesterol levels, elevated levels of inflammatory biomarkers, high blood pressure, diabetes, smoking (both active and passive smoking), obesity, genetic factors, family history, lifestyle habits, and an unhealthy diet. […] Atherogenesis is the developmental process of atheromatous plaques. It is characterized by a remodeling of arteries leading to subendothelial accumulation of fatty substances called plaques. The buildup of an atheromatous plaque is a slow process, developed over several years through a complex series of cellular events occurring within the arterial wall and in response to several local vascular circulating factors.

• #2 Inflammation in atherosclerosis: pathophysiology and mechanisms | Cell Death & Disease

  https://www.nature.com/articles/s41419-024-07166-8

  Atherosclerosis imposes a heavy burden on cardiovascular health due to its indispensable role in the pathogenesis of cardiovascular disease (CVD) such as coronary artery disease and heart failure. […] Ample clinical and experimental evidence has corroborated the vital role of inflammation in the pathophysiology of atherosclerosis. […] The pathophysiology of atherosclerosis is closely linked with inflammation and its transition to chronic inflammation. […] Monocytes/macrophages are at the center of driving plaque inflammation in atherosclerosis with broad and complicated molecular mechanisms, which are not fully deciphered. […] Current molecular findings on atherosclerotic inflammation are less likely to be translated into the clinic. […] The excessive retention or oxidation of LDL in the arterial subendothelial layer provokes monocyte generation from progenitor cells in the BM and their subsequent release into the circulation.

• #3 Inflammation in atherosclerosis: pathophysiology and mechanisms | Cell Death & Disease

  https://www.nature.com/articles/s41419-024-07166-8

  Atherosclerosis imposes a heavy burden on cardiovascular health due to its indispensable role in the pathogenesis of cardiovascular disease (CVD) such as coronary artery disease and heart failure. […] Ample clinical and experimental evidence has corroborated the vital role of inflammation in the pathophysiology of atherosclerosis. […] The pathophysiology of atherosclerosis is closely linked with inflammation and its transition to chronic inflammation. […] Monocytes/macrophages are at the center of driving plaque inflammation in atherosclerosis with broad and complicated molecular mechanisms, which are not fully deciphered. […] Current molecular findings on atherosclerotic inflammation are less likely to be translated into the clinic. […] The excessive retention or oxidation of LDL in the arterial subendothelial layer provokes monocyte generation from progenitor cells in the BM and their subsequent release into the circulation.

• #3 Atherosclerosis: Process, Indicators, Risk Factors and New Hopes

  https://pmc.ncbi.nlm.nih.gov/articles/PMC4258672/

  Atherosclerosis is the major cause of morbidities and mortalities worldwide. […] Inflammation has a crucial role in pathogenesis of atherosclerosis. The disease is accompanied by excessive fibrosis of the intima, fatty plaques formation, proliferation of smooth muscle cells, and migration of a group of cells such as monocytes, T cells, and platelets which are formed in response to inflammation. […] The oxidation of low density lipoprotein (LDL) to Ox-LDL indicates the first step of atherosclerosis in cardiovascular diseases. […] The pathogenesis factors involved in atherosclerosis have recently been cleared and the discovery of these factors has brought about new hopes for better prevention and treatment of atherosclerosis. […] Atherosclerosis is the result of hyperlipidemia and lipid oxidation and has always been a major cause of mortality in developed countries.

• #4 Atherosclerosis – Wikipedia

  https://en.wikipedia.org/wiki/Atherosclerosis

  Atherosclerosis is a pattern of the disease arteriosclerosis, characterized by development of abnormalities called lesions in walls of arteries. This is a chronic inflammatory disease involving many different cell types and is driven by elevated levels of cholesterol in the blood. These lesions may lead to narrowing of the arterial walls due to buildup of atheromatous plaques. […] The exact cause of atherosclerosis is unknown and is proposed to be multifactorial. Risk factors include abnormal cholesterol levels, elevated levels of inflammatory biomarkers, high blood pressure, diabetes, smoking (both active and passive smoking), obesity, genetic factors, family history, lifestyle habits, and an unhealthy diet. […] Atherogenesis is the developmental process of atheromatous plaques. It is characterized by a remodeling of arteries leading to subendothelial accumulation of fatty substances called plaques. The buildup of an atheromatous plaque is a slow process, developed over several years through a complex series of cellular events occurring within the arterial wall and in response to several local vascular circulating factors.

• #4 Mechanism of Hypercholesterolemia-Induced Atherosclerosis

  https://www.imrpress.com/journal/RCM/23/6/10.31083/j.rcm2306212/htm

  Hypercholesterolemia is involved in the development of atherosclerosis and is a risk factor for coronary artery disease, stroke, and peripheral vascular disease. This paper deals with the mechanism of development of hypercholesterolemic atherosclerosis. Hypercholesterolemia increases the formation of numerous atherogenic biomolecules including reactive oxygen species (ROS), proinflammatory cytokines [interleukin (IL)-1, IL-2, IL-6, IL-8, tumor necrosis factor-alpha (TNF-α)], expression of intercellular adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule-1 (VCAM-1), E-selectin, monocyte chemoattractant protein-1 (MCP-1), granulocyte macrophage-colony stimulating factor (GM-CSF) and numerous growth factors [insulin-like growth factor-1 (IGF-1), platelet-derived growth factor-1 (PDGF-1) and transforming growth factor-beta (TGF-β)]. ROS mildly oxidizes low-density lipoprotein-cholesterol (LDL-C) to form minimally modified LDL (MM-LDL) which is further oxidized to form oxidized LDL (OX-LDL). Hypercholesterolemia also activates nuclear factor-kappa-B (NF-κB). The above atherogenic biomolecules are involved in the development of atherosclerosis which has been described in detail. Hypercholesterolemia also assists in the development of atherosclerosis through AGE (advanced glycation end-products)-RAGE (receptor for AGE) axis and C-reactive protein (CRP). Hypercholesterolemia is associated with increases in AGE, oxidative stress [AGE/sRAGE (soluble receptor for AGE)] and C-reactive protein, and decreases in the sRAGE, which are known to be implicated in the development of atherosclerosis. In conclusion, hypercholesterolemia induces atherosclerosis through increases in atherogenic biomolecules, AGE-RAGE axis and CRP.

• #5 Pathophysiology of Atherosclerosis

  https://pmc.ncbi.nlm.nih.gov/articles/PMC8954705/

  Atherosclerosis is the main risk factor for cardiovascular disease (CVD), which is the leading cause of mortality worldwide. Atherosclerosis is initiated by endothelium activation and, followed by a cascade of events (accumulation of lipids, fibrous elements, and calcification), triggers the vessel narrowing and activation of inflammatory pathways. The resultant atheroma plaque, along with these processes, results in cardiovascular complications. […] Atherosclerosis initiates upon endothelial dysfunction accompanied by low-density lipoprotein (LDL) retention and its modification in the intima. Modified LDLs, together with additional atherogenic factors, promote the activation of ECs, leading to monocyte recruitment within the intima. Modified LDLs are avidly captured by differentiated monocytes and VSMC, which promote foam cell formation.

• #5 Atherosclerotic cardiovascular disease – Knowledge @ AMBOSS

  https://www.amboss.com/us/knowledge/atherosclerotic-cardiovascular-disease/

  Atherosclerosis is a multifactorial inflammatory disease of the intima, manifesting at points of hemodynamic shear stress. […] The pathogenesis of atherosclerosis is precipitated by endothelial damage, which leads to inflammation and the formation of atheromas in vessel walls. […] Chronic stress on the endothelium (e.g., due to arterial hypertension and turbulence) leads to endothelial cell dysfunction, which results in the invasion of inflammatory cells (mainly monocytes and lymphocytes) through the disrupted endothelial barrier. […] Adhesion of platelets to the damaged vessel wall leads to platelet release of inflammatory mediators (e.g., cytokines) and platelet-derived growth factor (PDGF). […] PDGF stimulates the migration and proliferation of smooth muscle cells (SMCs) in the tunica intima and mediates the differentiation of fibroblasts into myofibroblasts.

• #6 Pathophysiology of Atherosclerosis

  https://www.mdpi.com/1422-0067/23/6/3346

  Atherosclerosis is the main risk factor for cardiovascular disease (CVD), which is the leading cause of mortality worldwide. Atherosclerosis is initiated by endothelium activation and, followed by a cascade of events (accumulation of lipids, fibrous elements, and calcification), triggers the vessel narrowing and activation of inflammatory pathways. The resultant atheroma plaque, along with these processes, results in cardiovascular complications. […] Atherosclerosis initiates upon endothelial dysfunction accompanied by low-density lipoprotein (LDL) retention and its modification in the intima. Modified LDLs, together with additional atherogenic factors, promote the activation of ECs, leading to monocyte recruitment within the intima. Modified LDLs are avidly captured by differentiated monocytes and VSMC, which promote foam cell formation.

• #7 Pathophysiology of Atherosclerosis

  https://pmc.ncbi.nlm.nih.gov/articles/PMC8954705/

  Disruption of the mechanisms involved in vascular homeostasis regulation leads to endothelial dysfunction. Briefly, when ECs lose their ability to maintain homeostasis, vessel walls are predisposed to vasoconstriction, lipid infiltration, leukocyte adhesion, platelet activation, and oxidative stress, among other things. Together, these induce an inflammatory response that is considered the first step of atheromatous plaque formation: the fatty streak. […] Hemodynamic forces constitute a local risk factor of atherogenesis, as they promote endothelial dysfunction. […] Endothelial dysfunction is also explained through a reduction in NO bioavailability. NO is synthesized from L-arginine in ECs in a reaction catalyzed by eNOS and diffuses across cell membranes, reaching the smooth muscle tissue of the artery wall. NO promotes smooth muscle fiber relaxation, known as endothelium-dependent vasodilatation, and is considered an athero-protective molecule, because it counteracts atherogenesis and its complications.

• #8 Pathophysiology of Atherosclerosis

  https://www.mdpi.com/1422-0067/23/6/3346

  Disruption of the mechanisms involved in vascular homeostasis regulation leads to endothelial dysfunction. Briefly, when ECs lose their ability to maintain homeostasis, vessel walls are predisposed to vasoconstriction, lipid infiltration, leukocyte adhesion, platelet activation, and oxidative stress, among other things. Together, these induce an inflammatory response that is considered the first step of atheromatous plaque formation: the fatty streak. […] Hemodynamic forces constitute a local risk factor of atherogenesis, as they promote endothelial dysfunction. […] Endothelial dysfunction is also explained through a reduction in NO bioavailability. NO is synthesized from L-arginine in ECs in a reaction catalyzed by eNOS and diffuses across cell membranes, reaching the smooth muscle tissue of the artery wall. NO promotes smooth muscle fiber relaxation, known as endothelium-dependent vasodilatation, and is considered an athero-protective molecule, because it counteracts atherogenesis and its complications.

• #9 Pathophysiology of Atherosclerosis

  https://pmc.ncbi.nlm.nih.gov/articles/PMC8954705/

  Disruption of the mechanisms involved in vascular homeostasis regulation leads to endothelial dysfunction. Briefly, when ECs lose their ability to maintain homeostasis, vessel walls are predisposed to vasoconstriction, lipid infiltration, leukocyte adhesion, platelet activation, and oxidative stress, among other things. Together, these induce an inflammatory response that is considered the first step of atheromatous plaque formation: the fatty streak. […] Hemodynamic forces constitute a local risk factor of atherogenesis, as they promote endothelial dysfunction. […] Endothelial dysfunction is also explained through a reduction in NO bioavailability. NO is synthesized from L-arginine in ECs in a reaction catalyzed by eNOS and diffuses across cell membranes, reaching the smooth muscle tissue of the artery wall. NO promotes smooth muscle fiber relaxation, known as endothelium-dependent vasodilatation, and is considered an athero-protective molecule, because it counteracts atherogenesis and its complications.

• #10 Pathophysiology of Atherosclerosis

  https://www.mdpi.com/1422-0067/23/6/3346

  Disruption of the mechanisms involved in vascular homeostasis regulation leads to endothelial dysfunction. Briefly, when ECs lose their ability to maintain homeostasis, vessel walls are predisposed to vasoconstriction, lipid infiltration, leukocyte adhesion, platelet activation, and oxidative stress, among other things. Together, these induce an inflammatory response that is considered the first step of atheromatous plaque formation: the fatty streak. […] Hemodynamic forces constitute a local risk factor of atherogenesis, as they promote endothelial dysfunction. […] Endothelial dysfunction is also explained through a reduction in NO bioavailability. NO is synthesized from L-arginine in ECs in a reaction catalyzed by eNOS and diffuses across cell membranes, reaching the smooth muscle tissue of the artery wall. NO promotes smooth muscle fiber relaxation, known as endothelium-dependent vasodilatation, and is considered an athero-protective molecule, because it counteracts atherogenesis and its complications.

• #11 Atherosclerosis: Process, Indicators, Risk Factors and New Hopes

  https://pmc.ncbi.nlm.nih.gov/articles/PMC4258672/

  The starting point of this process is the damage caused by combination of unsaturated lipids of plasma or arterial membrane with oxygen or side products of their oxidation. […] The produced aldehydes bond with amino groups of ApoB-100. […] Oxidation also converts phosphatidylcholine to lysophosphatidylcholine and produces sterols from cholesterol esters in lipid core of LDL. […] Nitric oxide is produced in the endothelium and rapidly leaks to reach to the molecular targets in the vascular walls and vascular channels. […] Nitric oxide has anti-atherogenic effects in addition to vascular tone adjustment capability. […] Inflammatory mechanisms have a pivotal role in all steps of atherosclerosis. […] C-reactive protein is a factor related to lipoprotein deposition and complement system activity in atherosclerotic plaques.

• #12 What is the role of lipids in atherosclerosis and how low should we decrease lipid levels?

  https://www.escardio.org/Journals/E-Journal-of-Cardiology-Practice/Volume-18/what-is-the-role-of-lipids-in-atherosclerosis-and-how-low-should-we-decrease-lip

  According to the response-to-retention concept, the key initiating event in atherogenesis is the retention of these cholesterol-rich apoB-containing lipoproteins within the arterial wall, particularly in the presence of endothelial dysfunction. […] Following their retention in the arterial wall, lipoproteins undergo modifications and ultimately trigger a series of maladaptive responses that accelerate further lipoprotein retention and cause further plaque progression. […] This process is facilitated by modification of the LDL particle by non-oxidative alteration, oxidation, glycosylation, or glycooxidation. […] Retained LDL particles promote inflammatory and immune changes via cytokine release from macrophages, promoting further recruitment of immuno-inflammatory cells. […] The initiation and progression of atherosclerosis is also modified by the susceptibility of retained lipoproteins to undergo modifications and induce maladaptive cellular responses within the arterial wall.

• #13 Pathophysiology of Atherosclerosis

  https://pmc.ncbi.nlm.nih.gov/articles/PMC8954705/

  Accumulation of LDL in plasma favors transendothelial infiltration of circulating LDLs to the intima. […] Once in the subendothelial space, trapped LDL particles are oxidized, a process facilitated by the absence of protective plasma antioxidants. Oxidized LDLs are key inflammatory components that promote atherosclerotic plaque development, as they contain oxidized lipids and products derived from their degradation that contribute to the physiopathology of the disease. […] Endothelial stimulation, also known as endothelial type I activation, occurs when inflammatory agents induce a response such as a change in microvascular tone, permeability, or leukocyte diapedesis. […] Activated ECs induce selective monocyte recruitment into the intima. […] The necrotic core constitutes the nucleus of the atherosclerotic plaques. Covered by the fibrous cap, the necrotic core consists of a lipid-laden hipocellular region with reduced supporting collagen.

• #14 Pathophysiology of Atherosclerosis

  https://pmc.ncbi.nlm.nih.gov/articles/PMC8954705/

  Accumulation of LDL in plasma favors transendothelial infiltration of circulating LDLs to the intima. […] Once in the subendothelial space, trapped LDL particles are oxidized, a process facilitated by the absence of protective plasma antioxidants. Oxidized LDLs are key inflammatory components that promote atherosclerotic plaque development, as they contain oxidized lipids and products derived from their degradation that contribute to the physiopathology of the disease. […] Endothelial stimulation, also known as endothelial type I activation, occurs when inflammatory agents induce a response such as a change in microvascular tone, permeability, or leukocyte diapedesis. […] Activated ECs induce selective monocyte recruitment into the intima. […] The necrotic core constitutes the nucleus of the atherosclerotic plaques. Covered by the fibrous cap, the necrotic core consists of a lipid-laden hipocellular region with reduced supporting collagen.

• #15 Inflammation in atherosclerosis: pathophysiology and mechanisms | Cell Death & Disease

  https://www.nature.com/articles/s41419-024-07166-8

  These findings corroborate the indispensable role of inflammation in the progression of atherosclerosis. […] One of the key events in atherogenesis is the cumulative oxidation of aggregated LDL within the plaque. […] The oxidation of LDL promotes its uptake by macrophages in the intimal layer. […] Hence, beyond the primary events, inflammation plays a decisive role in the exacerbation of the plaque and the progression of atherosclerosis. […] The hypoxia-induced activation of HIF-1 in macrophages may lead to the downregulation of PPAR-, thus driving plaque inflammation by reactivating proinflammatory genes and the repression of anti-inflammatory genes. […] Hypoxia activates the HIF-1 transcription factor in plaque macrophages, leading to the transactivation of proinflammatory genes such as cytokines (e.g. MIF).

• #16 Inflammation in atherosclerosis: pathophysiology and mechanisms | Cell Death & Disease

  https://www.nature.com/articles/s41419-024-07166-8

  These findings corroborate the indispensable role of inflammation in the progression of atherosclerosis. […] One of the key events in atherogenesis is the cumulative oxidation of aggregated LDL within the plaque. […] The oxidation of LDL promotes its uptake by macrophages in the intimal layer. […] Hence, beyond the primary events, inflammation plays a decisive role in the exacerbation of the plaque and the progression of atherosclerosis. […] The hypoxia-induced activation of HIF-1 in macrophages may lead to the downregulation of PPAR-, thus driving plaque inflammation by reactivating proinflammatory genes and the repression of anti-inflammatory genes. […] Hypoxia activates the HIF-1 transcription factor in plaque macrophages, leading to the transactivation of proinflammatory genes such as cytokines (e.g. MIF).

• #17 Atherosclerosis: Process, Indicators, Risk Factors and New Hopes

  https://pmc.ncbi.nlm.nih.gov/articles/PMC4258672/

  The starting point of this process is the damage caused by combination of unsaturated lipids of plasma or arterial membrane with oxygen or side products of their oxidation. […] The produced aldehydes bond with amino groups of ApoB-100. […] Oxidation also converts phosphatidylcholine to lysophosphatidylcholine and produces sterols from cholesterol esters in lipid core of LDL. […] Nitric oxide is produced in the endothelium and rapidly leaks to reach to the molecular targets in the vascular walls and vascular channels. […] Nitric oxide has anti-atherogenic effects in addition to vascular tone adjustment capability. […] Inflammatory mechanisms have a pivotal role in all steps of atherosclerosis. […] C-reactive protein is a factor related to lipoprotein deposition and complement system activity in atherosclerotic plaques.

• #18 Atherosclerosis: Process, Indicators, Risk Factors and New Hopes

  https://pmc.ncbi.nlm.nih.gov/articles/PMC4258672/

  The starting point of this process is the damage caused by combination of unsaturated lipids of plasma or arterial membrane with oxygen or side products of their oxidation. […] The produced aldehydes bond with amino groups of ApoB-100. […] Oxidation also converts phosphatidylcholine to lysophosphatidylcholine and produces sterols from cholesterol esters in lipid core of LDL. […] Nitric oxide is produced in the endothelium and rapidly leaks to reach to the molecular targets in the vascular walls and vascular channels. […] Nitric oxide has anti-atherogenic effects in addition to vascular tone adjustment capability. […] Inflammatory mechanisms have a pivotal role in all steps of atherosclerosis. […] C-reactive protein is a factor related to lipoprotein deposition and complement system activity in atherosclerotic plaques.

• #19 Atherosclerosis: Process, Indicators, Risk Factors and New Hopes

  https://pmc.ncbi.nlm.nih.gov/articles/PMC4258672/

  The starting point of this process is the damage caused by combination of unsaturated lipids of plasma or arterial membrane with oxygen or side products of their oxidation. […] The produced aldehydes bond with amino groups of ApoB-100. […] Oxidation also converts phosphatidylcholine to lysophosphatidylcholine and produces sterols from cholesterol esters in lipid core of LDL. […] Nitric oxide is produced in the endothelium and rapidly leaks to reach to the molecular targets in the vascular walls and vascular channels. […] Nitric oxide has anti-atherogenic effects in addition to vascular tone adjustment capability. […] Inflammatory mechanisms have a pivotal role in all steps of atherosclerosis. […] C-reactive protein is a factor related to lipoprotein deposition and complement system activity in atherosclerotic plaques.

• #20 Pathophysiology of Atherosclerosis

  https://pmc.ncbi.nlm.nih.gov/articles/PMC8954705/

  Accumulation of LDL in plasma favors transendothelial infiltration of circulating LDLs to the intima. […] Once in the subendothelial space, trapped LDL particles are oxidized, a process facilitated by the absence of protective plasma antioxidants. Oxidized LDLs are key inflammatory components that promote atherosclerotic plaque development, as they contain oxidized lipids and products derived from their degradation that contribute to the physiopathology of the disease. […] Endothelial stimulation, also known as endothelial type I activation, occurs when inflammatory agents induce a response such as a change in microvascular tone, permeability, or leukocyte diapedesis. […] Activated ECs induce selective monocyte recruitment into the intima. […] The necrotic core constitutes the nucleus of the atherosclerotic plaques. Covered by the fibrous cap, the necrotic core consists of a lipid-laden hipocellular region with reduced supporting collagen.

• #21 Pathophysiology of Atherosclerosis

  https://pmc.ncbi.nlm.nih.gov/articles/PMC8954705/

  Accumulation of LDL in plasma favors transendothelial infiltration of circulating LDLs to the intima. […] Once in the subendothelial space, trapped LDL particles are oxidized, a process facilitated by the absence of protective plasma antioxidants. Oxidized LDLs are key inflammatory components that promote atherosclerotic plaque development, as they contain oxidized lipids and products derived from their degradation that contribute to the physiopathology of the disease. […] Endothelial stimulation, also known as endothelial type I activation, occurs when inflammatory agents induce a response such as a change in microvascular tone, permeability, or leukocyte diapedesis. […] Activated ECs induce selective monocyte recruitment into the intima. […] The necrotic core constitutes the nucleus of the atherosclerotic plaques. Covered by the fibrous cap, the necrotic core consists of a lipid-laden hipocellular region with reduced supporting collagen.

• #22 Inflammation in atherosclerosis: pathophysiology and mechanisms | Cell Death & Disease

  https://www.nature.com/articles/s41419-024-07166-8

  Atherosclerosis imposes a heavy burden on cardiovascular health due to its indispensable role in the pathogenesis of cardiovascular disease (CVD) such as coronary artery disease and heart failure. […] Ample clinical and experimental evidence has corroborated the vital role of inflammation in the pathophysiology of atherosclerosis. […] The pathophysiology of atherosclerosis is closely linked with inflammation and its transition to chronic inflammation. […] Monocytes/macrophages are at the center of driving plaque inflammation in atherosclerosis with broad and complicated molecular mechanisms, which are not fully deciphered. […] Current molecular findings on atherosclerotic inflammation are less likely to be translated into the clinic. […] The excessive retention or oxidation of LDL in the arterial subendothelial layer provokes monocyte generation from progenitor cells in the BM and their subsequent release into the circulation.

• #23 Inflammation in atherosclerosis: pathophysiology and mechanisms | Cell Death & Disease

  https://www.nature.com/articles/s41419-024-07166-8

  Atherosclerosis imposes a heavy burden on cardiovascular health due to its indispensable role in the pathogenesis of cardiovascular disease (CVD) such as coronary artery disease and heart failure. […] Ample clinical and experimental evidence has corroborated the vital role of inflammation in the pathophysiology of atherosclerosis. […] The pathophysiology of atherosclerosis is closely linked with inflammation and its transition to chronic inflammation. […] Monocytes/macrophages are at the center of driving plaque inflammation in atherosclerosis with broad and complicated molecular mechanisms, which are not fully deciphered. […] Current molecular findings on atherosclerotic inflammation are less likely to be translated into the clinic. […] The excessive retention or oxidation of LDL in the arterial subendothelial layer provokes monocyte generation from progenitor cells in the BM and their subsequent release into the circulation.

• #24 Inflammation in atherosclerosis: pathophysiology and mechanisms | Cell Death & Disease

  https://www.nature.com/articles/s41419-024-07166-8

  Inflammatory macrophages release chemokines/cytokines, which promote plaque inflammation. […] As the plaque grows, it becomes unstable and may rupture. […] Due to the inflammatory milieu of the plaque, procoagulant factors are activated and fibrin production increases. […] While efferocytosis prevents inflammation and plaque growth, the impaired efferocytosis of apoptotic/necrotic bodies may lead to further deposition of macrophages/foam cells in the plaque. […] Due to the inflammatory conditions of the plaque, monocytes differentiate into DCs, which infiltrate the endothelium and release proinflammatory cytokines that promote inflammation and atherosclerosis. […] Stable plaques are featured by chronic low-grade inflammation, while unstable plaques exhibit active inflammation, which further promotes plaque rupture and vulnerability by thinning the fibrous cap.

• #25 Inflammation in atherosclerosis: pathophysiology and mechanisms | Cell Death & Disease

  https://www.nature.com/articles/s41419-024-07166-8

  Inflammatory macrophages release chemokines/cytokines, which promote plaque inflammation. […] As the plaque grows, it becomes unstable and may rupture. […] Due to the inflammatory milieu of the plaque, procoagulant factors are activated and fibrin production increases. […] While efferocytosis prevents inflammation and plaque growth, the impaired efferocytosis of apoptotic/necrotic bodies may lead to further deposition of macrophages/foam cells in the plaque. […] Due to the inflammatory conditions of the plaque, monocytes differentiate into DCs, which infiltrate the endothelium and release proinflammatory cytokines that promote inflammation and atherosclerosis. […] Stable plaques are featured by chronic low-grade inflammation, while unstable plaques exhibit active inflammation, which further promotes plaque rupture and vulnerability by thinning the fibrous cap.

• #26 Inflammation in atherosclerosis: pathophysiology and mechanisms | Cell Death & Disease

  https://www.nature.com/articles/s41419-024-07166-8

  Inflammatory macrophages release chemokines/cytokines, which promote plaque inflammation. […] As the plaque grows, it becomes unstable and may rupture. […] Due to the inflammatory milieu of the plaque, procoagulant factors are activated and fibrin production increases. […] While efferocytosis prevents inflammation and plaque growth, the impaired efferocytosis of apoptotic/necrotic bodies may lead to further deposition of macrophages/foam cells in the plaque. […] Due to the inflammatory conditions of the plaque, monocytes differentiate into DCs, which infiltrate the endothelium and release proinflammatory cytokines that promote inflammation and atherosclerosis. […] Stable plaques are featured by chronic low-grade inflammation, while unstable plaques exhibit active inflammation, which further promotes plaque rupture and vulnerability by thinning the fibrous cap.

• #27 Inflammation in atherosclerosis: pathophysiology and mechanisms | Cell Death & Disease

  https://www.nature.com/articles/s41419-024-07166-8

  Inflammatory macrophages release chemokines/cytokines, which promote plaque inflammation. […] As the plaque grows, it becomes unstable and may rupture. […] Due to the inflammatory milieu of the plaque, procoagulant factors are activated and fibrin production increases. […] While efferocytosis prevents inflammation and plaque growth, the impaired efferocytosis of apoptotic/necrotic bodies may lead to further deposition of macrophages/foam cells in the plaque. […] Due to the inflammatory conditions of the plaque, monocytes differentiate into DCs, which infiltrate the endothelium and release proinflammatory cytokines that promote inflammation and atherosclerosis. […] Stable plaques are featured by chronic low-grade inflammation, while unstable plaques exhibit active inflammation, which further promotes plaque rupture and vulnerability by thinning the fibrous cap.

• #28 Inflammation in atherosclerosis: pathophysiology and mechanisms | Cell Death & Disease

  https://www.nature.com/articles/s41419-024-07166-8

  Inflammatory macrophages release chemokines/cytokines, which promote plaque inflammation. […] As the plaque grows, it becomes unstable and may rupture. […] Due to the inflammatory milieu of the plaque, procoagulant factors are activated and fibrin production increases. […] While efferocytosis prevents inflammation and plaque growth, the impaired efferocytosis of apoptotic/necrotic bodies may lead to further deposition of macrophages/foam cells in the plaque. […] Due to the inflammatory conditions of the plaque, monocytes differentiate into DCs, which infiltrate the endothelium and release proinflammatory cytokines that promote inflammation and atherosclerosis. […] Stable plaques are featured by chronic low-grade inflammation, while unstable plaques exhibit active inflammation, which further promotes plaque rupture and vulnerability by thinning the fibrous cap.

• #29 Mechanism of Hypercholesterolemia-Induced Atherosclerosis

  https://www.imrpress.com/journal/RCM/23/6/10.31083/j.rcm2306212/htm

  Hypercholesterolemia is involved in the development of atherosclerosis and is a risk factor for coronary artery disease, stroke, and peripheral vascular disease. This paper deals with the mechanism of development of hypercholesterolemic atherosclerosis. Hypercholesterolemia increases the formation of numerous atherogenic biomolecules including reactive oxygen species (ROS), proinflammatory cytokines [interleukin (IL)-1, IL-2, IL-6, IL-8, tumor necrosis factor-alpha (TNF-α)], expression of intercellular adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule-1 (VCAM-1), E-selectin, monocyte chemoattractant protein-1 (MCP-1), granulocyte macrophage-colony stimulating factor (GM-CSF) and numerous growth factors [insulin-like growth factor-1 (IGF-1), platelet-derived growth factor-1 (PDGF-1) and transforming growth factor-beta (TGF-β)]. ROS mildly oxidizes low-density lipoprotein-cholesterol (LDL-C) to form minimally modified LDL (MM-LDL) which is further oxidized to form oxidized LDL (OX-LDL). Hypercholesterolemia also activates nuclear factor-kappa-B (NF-κB). The above atherogenic biomolecules are involved in the development of atherosclerosis which has been described in detail. Hypercholesterolemia also assists in the development of atherosclerosis through AGE (advanced glycation end-products)-RAGE (receptor for AGE) axis and C-reactive protein (CRP). Hypercholesterolemia is associated with increases in AGE, oxidative stress [AGE/sRAGE (soluble receptor for AGE)] and C-reactive protein, and decreases in the sRAGE, which are known to be implicated in the development of atherosclerosis. In conclusion, hypercholesterolemia induces atherosclerosis through increases in atherogenic biomolecules, AGE-RAGE axis and CRP.

• #30 Mechanism of Hypercholesterolemia-Induced Atherosclerosis

  https://www.imrpress.com/journal/RCM/23/6/10.31083/j.rcm2306212/htm

  Hypercholesterolemia is involved in the development of atherosclerosis and is a risk factor for coronary artery disease, stroke, and peripheral vascular disease. This paper deals with the mechanism of development of hypercholesterolemic atherosclerosis. Hypercholesterolemia increases the formation of numerous atherogenic biomolecules including reactive oxygen species (ROS), proinflammatory cytokines [interleukin (IL)-1, IL-2, IL-6, IL-8, tumor necrosis factor-alpha (TNF-α)], expression of intercellular adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule-1 (VCAM-1), E-selectin, monocyte chemoattractant protein-1 (MCP-1), granulocyte macrophage-colony stimulating factor (GM-CSF) and numerous growth factors [insulin-like growth factor-1 (IGF-1), platelet-derived growth factor-1 (PDGF-1) and transforming growth factor-beta (TGF-β)]. ROS mildly oxidizes low-density lipoprotein-cholesterol (LDL-C) to form minimally modified LDL (MM-LDL) which is further oxidized to form oxidized LDL (OX-LDL). Hypercholesterolemia also activates nuclear factor-kappa-B (NF-κB). The above atherogenic biomolecules are involved in the development of atherosclerosis which has been described in detail. Hypercholesterolemia also assists in the development of atherosclerosis through AGE (advanced glycation end-products)-RAGE (receptor for AGE) axis and C-reactive protein (CRP). Hypercholesterolemia is associated with increases in AGE, oxidative stress [AGE/sRAGE (soluble receptor for AGE)] and C-reactive protein, and decreases in the sRAGE, which are known to be implicated in the development of atherosclerosis. In conclusion, hypercholesterolemia induces atherosclerosis through increases in atherogenic biomolecules, AGE-RAGE axis and CRP.

• #31 Mechanism of Hypercholesterolemia-Induced Atherosclerosis

  https://www.imrpress.com/journal/RCM/23/6/10.31083/j.rcm2306212/htm

  Hypercholesterolemia-induced atherosclerosis is based on the oxidative hypothesis of atherosclerosis which has been accepted universally. The proposed mechanism of atherosclerosis produced by hypercholesterolemia is depicted in Fig. 2. Hypercholesterolemia augments the production of ROS and cytokines which increase the expression of CAM in endothelial cells. The early step in the development of atherosclerosis is adherence of monocytes to endothelial cells and which is achieved through CAM. CAM is involved in the rolling and adhesion of monocytes to the endothelial cells. Monocyte then transmigrates into subendothelial space. MM-LDL produce monocyte chemoattractant protein-1 (MCP-1) in endothelial cells and vascular smooth muscle cells. The migration of monocytes to the subendothelial space is assisted by MCP-1. OX-LDL increases the expression of cell adhesion molecules. OX-LDL directly enhances the migration of monocytes to subendothelial space. Immigrating monocytes into the subendothelial space have LDL receptor but the rate of uptake of native LDL is not enough to produce foam cells. MM-LDL stimulates endothelial cells to express MC-SF that enhances the monocyte differentiation to form tissue macrophages which develop receptors for OX-LDL. OX-LDL is a ligand for scavenger receptors which are expressed in tissue macrophages. OX-LDL is taken up by tissue macrophage to form foam cells. Foam cells are involved in formation of numerous growth factors which enhance vascular smooth muscle cell proliferation and migration and fibrous tissue synthesis which helps in the development and progression of atherosclerosis. There is a development of fatty streaks in full-fledged atherosclerosis.

• #32 Pathophysiology of Atherosclerosis

  https://pmc.ncbi.nlm.nih.gov/articles/PMC8954705/

  Disruption of the mechanisms involved in vascular homeostasis regulation leads to endothelial dysfunction. Briefly, when ECs lose their ability to maintain homeostasis, vessel walls are predisposed to vasoconstriction, lipid infiltration, leukocyte adhesion, platelet activation, and oxidative stress, among other things. Together, these induce an inflammatory response that is considered the first step of atheromatous plaque formation: the fatty streak. […] Hemodynamic forces constitute a local risk factor of atherogenesis, as they promote endothelial dysfunction. […] Endothelial dysfunction is also explained through a reduction in NO bioavailability. NO is synthesized from L-arginine in ECs in a reaction catalyzed by eNOS and diffuses across cell membranes, reaching the smooth muscle tissue of the artery wall. NO promotes smooth muscle fiber relaxation, known as endothelium-dependent vasodilatation, and is considered an athero-protective molecule, because it counteracts atherogenesis and its complications.

• #33 Pathophysiology of Atherosclerosis

  https://www.mdpi.com/1422-0067/23/6/3346

  Disruption of the mechanisms involved in vascular homeostasis regulation leads to endothelial dysfunction. Briefly, when ECs lose their ability to maintain homeostasis, vessel walls are predisposed to vasoconstriction, lipid infiltration, leukocyte adhesion, platelet activation, and oxidative stress, among other things. Together, these induce an inflammatory response that is considered the first step of atheromatous plaque formation: the fatty streak. […] Hemodynamic forces constitute a local risk factor of atherogenesis, as they promote endothelial dysfunction. […] Endothelial dysfunction is also explained through a reduction in NO bioavailability. NO is synthesized from L-arginine in ECs in a reaction catalyzed by eNOS and diffuses across cell membranes, reaching the smooth muscle tissue of the artery wall. NO promotes smooth muscle fiber relaxation, known as endothelium-dependent vasodilatation, and is considered an athero-protective molecule, because it counteracts atherogenesis and its complications.

• #34 Atherosclerosis: Process, Indicators, Risk Factors and New Hopes

  https://pmc.ncbi.nlm.nih.gov/articles/PMC4258672/

  Currently, atherosclerosis is a common disease in which fatty deposits called atheromatous plaques appear in the inner layers of arteries. […] Hyperlipidemia and hyperglycemia are related to increased oxidative damage, which affects antioxidant status and lipoprotein levels. […] Studies have shown that lipid lowering medicinal herbs can reduce the blood lipids especially after meals in addition to their antioxidant effects. […] The initial soft lesion is composed of foam cells and extracellular fat deposits and a small number of platelets. […] Severe damage to vascular tissue happens when adjacent SMC and endothelial cells secret small peptides such as cytokines and growth factors such as interleukin 1 (IL-1), and TNF (which causes cell growth). […] These processes weaken the formed plaque shaped fibrous cap and can destroy it.

• #35 Mechanism of Hypercholesterolemia-Induced Atherosclerosis

  https://www.imrpress.com/journal/RCM/23/6/10.31083/j.rcm2306212/htm

  Hypercholesterolemia-induced atherosclerosis is based on the oxidative hypothesis of atherosclerosis which has been accepted universally. The proposed mechanism of atherosclerosis produced by hypercholesterolemia is depicted in Fig. 2. Hypercholesterolemia augments the production of ROS and cytokines which increase the expression of CAM in endothelial cells. The early step in the development of atherosclerosis is adherence of monocytes to endothelial cells and which is achieved through CAM. CAM is involved in the rolling and adhesion of monocytes to the endothelial cells. Monocyte then transmigrates into subendothelial space. MM-LDL produce monocyte chemoattractant protein-1 (MCP-1) in endothelial cells and vascular smooth muscle cells. The migration of monocytes to the subendothelial space is assisted by MCP-1. OX-LDL increases the expression of cell adhesion molecules. OX-LDL directly enhances the migration of monocytes to subendothelial space. Immigrating monocytes into the subendothelial space have LDL receptor but the rate of uptake of native LDL is not enough to produce foam cells. MM-LDL stimulates endothelial cells to express MC-SF that enhances the monocyte differentiation to form tissue macrophages which develop receptors for OX-LDL. OX-LDL is a ligand for scavenger receptors which are expressed in tissue macrophages. OX-LDL is taken up by tissue macrophage to form foam cells. Foam cells are involved in formation of numerous growth factors which enhance vascular smooth muscle cell proliferation and migration and fibrous tissue synthesis which helps in the development and progression of atherosclerosis. There is a development of fatty streaks in full-fledged atherosclerosis.

• #36 Mechanism of Hypercholesterolemia-Induced Atherosclerosis

  https://www.imrpress.com/journal/RCM/23/6/10.31083/j.rcm2306212/htm

  Hypercholesterolemia-induced atherosclerosis is based on the oxidative hypothesis of atherosclerosis which has been accepted universally. The proposed mechanism of atherosclerosis produced by hypercholesterolemia is depicted in Fig. 2. Hypercholesterolemia augments the production of ROS and cytokines which increase the expression of CAM in endothelial cells. The early step in the development of atherosclerosis is adherence of monocytes to endothelial cells and which is achieved through CAM. CAM is involved in the rolling and adhesion of monocytes to the endothelial cells. Monocyte then transmigrates into subendothelial space. MM-LDL produce monocyte chemoattractant protein-1 (MCP-1) in endothelial cells and vascular smooth muscle cells. The migration of monocytes to the subendothelial space is assisted by MCP-1. OX-LDL increases the expression of cell adhesion molecules. OX-LDL directly enhances the migration of monocytes to subendothelial space. Immigrating monocytes into the subendothelial space have LDL receptor but the rate of uptake of native LDL is not enough to produce foam cells. MM-LDL stimulates endothelial cells to express MC-SF that enhances the monocyte differentiation to form tissue macrophages which develop receptors for OX-LDL. OX-LDL is a ligand for scavenger receptors which are expressed in tissue macrophages. OX-LDL is taken up by tissue macrophage to form foam cells. Foam cells are involved in formation of numerous growth factors which enhance vascular smooth muscle cell proliferation and migration and fibrous tissue synthesis which helps in the development and progression of atherosclerosis. There is a development of fatty streaks in full-fledged atherosclerosis.

• #37 Mechanism of Hypercholesterolemia-Induced Atherosclerosis

  https://www.imrpress.com/journal/RCM/23/6/10.31083/j.rcm2306212/htm

  Hypercholesterolemia-induced atherosclerosis is based on the oxidative hypothesis of atherosclerosis which has been accepted universally. The proposed mechanism of atherosclerosis produced by hypercholesterolemia is depicted in Fig. 2. Hypercholesterolemia augments the production of ROS and cytokines which increase the expression of CAM in endothelial cells. The early step in the development of atherosclerosis is adherence of monocytes to endothelial cells and which is achieved through CAM. CAM is involved in the rolling and adhesion of monocytes to the endothelial cells. Monocyte then transmigrates into subendothelial space. MM-LDL produce monocyte chemoattractant protein-1 (MCP-1) in endothelial cells and vascular smooth muscle cells. The migration of monocytes to the subendothelial space is assisted by MCP-1. OX-LDL increases the expression of cell adhesion molecules. OX-LDL directly enhances the migration of monocytes to subendothelial space. Immigrating monocytes into the subendothelial space have LDL receptor but the rate of uptake of native LDL is not enough to produce foam cells. MM-LDL stimulates endothelial cells to express MC-SF that enhances the monocyte differentiation to form tissue macrophages which develop receptors for OX-LDL. OX-LDL is a ligand for scavenger receptors which are expressed in tissue macrophages. OX-LDL is taken up by tissue macrophage to form foam cells. Foam cells are involved in formation of numerous growth factors which enhance vascular smooth muscle cell proliferation and migration and fibrous tissue synthesis which helps in the development and progression of atherosclerosis. There is a development of fatty streaks in full-fledged atherosclerosis.

• #38 Pathophysiology of Atherosclerosis

  https://www.mdpi.com/1422-0067/23/6/3346

  Atherosclerosis is a disease that is characterized by the accumulation of lipids, fibrous elements, and calcification within the large arteries. This process is initiated by endothelium activation, followed by a cascade of events, which implies the vessel narrowing and activation of inflammatory pathways leading to atheroma plaque formation. […] The fibrous cap is a subendothelial barrier between the lumen of the vessel and the atherosclerotic necrotic core consisting of VSMCs that have migrated to the luminal side of the artery and extracellular matrix (ECM) derived from VSMCs. The role of the fibrous cap is to serve as a structural support to avoid the exposure of prothrombotic material of the core that otherwise would trigger thrombosis. […] The necrotic core constitutes the nucleus of the atherosclerotic plaques. Covered by the fibrous cap, the necrotic core consists of a lipid-laden hipocellular region with reduced supporting collagen.

• #39 Pathophysiology of Atherosclerosis

  https://pmc.ncbi.nlm.nih.gov/articles/PMC8954705/

  Accumulation of LDL in plasma favors transendothelial infiltration of circulating LDLs to the intima. […] Once in the subendothelial space, trapped LDL particles are oxidized, a process facilitated by the absence of protective plasma antioxidants. Oxidized LDLs are key inflammatory components that promote atherosclerotic plaque development, as they contain oxidized lipids and products derived from their degradation that contribute to the physiopathology of the disease. […] Endothelial stimulation, also known as endothelial type I activation, occurs when inflammatory agents induce a response such as a change in microvascular tone, permeability, or leukocyte diapedesis. […] Activated ECs induce selective monocyte recruitment into the intima. […] The necrotic core constitutes the nucleus of the atherosclerotic plaques. Covered by the fibrous cap, the necrotic core consists of a lipid-laden hipocellular region with reduced supporting collagen.

• #40 Pathophysiology of Atherosclerosis

  https://www.mdpi.com/1422-0067/23/6/3346

  Atherosclerosis is a disease that is characterized by the accumulation of lipids, fibrous elements, and calcification within the large arteries. This process is initiated by endothelium activation, followed by a cascade of events, which implies the vessel narrowing and activation of inflammatory pathways leading to atheroma plaque formation. […] The fibrous cap is a subendothelial barrier between the lumen of the vessel and the atherosclerotic necrotic core consisting of VSMCs that have migrated to the luminal side of the artery and extracellular matrix (ECM) derived from VSMCs. The role of the fibrous cap is to serve as a structural support to avoid the exposure of prothrombotic material of the core that otherwise would trigger thrombosis. […] The necrotic core constitutes the nucleus of the atherosclerotic plaques. Covered by the fibrous cap, the necrotic core consists of a lipid-laden hipocellular region with reduced supporting collagen.

• #41 Pathophysiology of Atherosclerosis

  https://pmc.ncbi.nlm.nih.gov/articles/PMC8954705/

  Atheroma plaque calcification is another hallmark of advanced atherosclerosis. It exists as a bone-like formation within the plaque and is initiated in inflammatory regions with a local decrease in collagen fibers. […] A plaque is considered vulnerable when the lesion shows a large necrotic core, a thin fibrous cap, and an increased inflammatory response due to the continuous exposure to the pro-atherogenic milieu. […] When the plaque fissures or ruptures, the subendothelial space is exposed to blood, triggering a coagulation process to cover the wound.

• #42 Pathophysiology of Atherosclerosis

  https://www.mdpi.com/1422-0067/23/6/3346

  Atheroma plaque calcification is another hallmark of advanced atherosclerosis. It exists as a bone-like formation within the plaque and is initiated in inflammatory regions with a local decrease in collagen fibers. […] The mechanisms involved in plaque rupture are not completely understood, but plaque vulnerability is associated with fibrous cap thickness, necrotic core development, and the inflammatory response. […] Several inflammation processes participate in all phases of atherosclerosis. At early stages of atherosclerosis, LDLs accumulate in the subendothelial region, where they become modified.

• #43 Pathophysiology of Atherosclerosis

  https://pmc.ncbi.nlm.nih.gov/articles/PMC8954705/

  Atheroma plaque calcification is another hallmark of advanced atherosclerosis. It exists as a bone-like formation within the plaque and is initiated in inflammatory regions with a local decrease in collagen fibers. […] A plaque is considered vulnerable when the lesion shows a large necrotic core, a thin fibrous cap, and an increased inflammatory response due to the continuous exposure to the pro-atherogenic milieu. […] When the plaque fissures or ruptures, the subendothelial space is exposed to blood, triggering a coagulation process to cover the wound.

• #44 Pathophysiology of Atherosclerosis

  https://www.mdpi.com/1422-0067/23/6/3346

  Atheroma plaque calcification is another hallmark of advanced atherosclerosis. It exists as a bone-like formation within the plaque and is initiated in inflammatory regions with a local decrease in collagen fibers. […] The mechanisms involved in plaque rupture are not completely understood, but plaque vulnerability is associated with fibrous cap thickness, necrotic core development, and the inflammatory response. […] Several inflammation processes participate in all phases of atherosclerosis. At early stages of atherosclerosis, LDLs accumulate in the subendothelial region, where they become modified.

• #45 Pathophysiology of Atherosclerosis

  https://pmc.ncbi.nlm.nih.gov/articles/PMC8954705/

  Atheroma plaque calcification is another hallmark of advanced atherosclerosis. It exists as a bone-like formation within the plaque and is initiated in inflammatory regions with a local decrease in collagen fibers. […] A plaque is considered vulnerable when the lesion shows a large necrotic core, a thin fibrous cap, and an increased inflammatory response due to the continuous exposure to the pro-atherogenic milieu. […] When the plaque fissures or ruptures, the subendothelial space is exposed to blood, triggering a coagulation process to cover the wound.

• #46 Atherosclerotic cardiovascular disease – Knowledge @ AMBOSS

  https://www.amboss.com/us/knowledge/atherosclerotic-cardiovascular-disease/

  Inflammation of the vessel wall occurs, and macrophages and SMCs ingest cholesterol from oxidized LDL, transforming into foam cells (macrophages filled with lipid droplets). […] Foam cells accumulate to form fatty streaks (early atherosclerotic lesions). […] Lipid-laden macrophages and SMCs produce extracellular matrix (e.g., collagen) deposition, leading to the development of a fibrous plaque (atheroma). […] Inflammatory cells in the atheroma (e.g., macrophages) secrete matrix metalloproteinases, weakening the fibrous cap of the plaque due to the breakdown of extracellular matrix, which can result in minor stress rupturing the fibrous cap. […] Calcification of the intima occurs, and the amount and pattern of calcification affect the risk of complications. […] Plaque rupture exposes thrombogenic material (e.g., collagen), leading to thrombus formation with vascular occlusion or spreading of thrombogenic material.

• #47 Pathophysiology of Atherosclerosis

  https://www.mdpi.com/1422-0067/23/6/3346

  Atheroma plaque calcification is another hallmark of advanced atherosclerosis. It exists as a bone-like formation within the plaque and is initiated in inflammatory regions with a local decrease in collagen fibers. […] The mechanisms involved in plaque rupture are not completely understood, but plaque vulnerability is associated with fibrous cap thickness, necrotic core development, and the inflammatory response. […] Several inflammation processes participate in all phases of atherosclerosis. At early stages of atherosclerosis, LDLs accumulate in the subendothelial region, where they become modified.

• #48 Novel Insights into the Molecular Mechanisms of Atherosclerosis

  https://www.mdpi.com/1422-0067/24/17/13434

  Inflammation starts with inflammasomes, which are innate immunological signaling complexes that are a significant modulator of IL-1 family cytokine production in atherosclerosis, contributing to the vascular inflammatory response that drives the development and progression of atherosclerosis. […] The pathogeneses of atherosclerosis and diabetes are closely related. Diabetes has been shown to be a triggering factor for atherosclerosis due to dyslipidemia, hyperglycemia, oxidative stress, and chronic inflammation. […] Atherosclerosis results in CVD, which can take the form of ischemic heart disease, stroke, or other vascular diseases. […] Atherosclerosis is chronic arterial inflammation caused by both conventional and unconventional risk factors that result in plaque development in the vascular intima.

• #49 Inflammation in atherosclerosis: pathophysiology and mechanisms | Cell Death & Disease

  https://www.nature.com/articles/s41419-024-07166-8

  Inflammatory macrophages release chemokines/cytokines, which promote plaque inflammation. […] As the plaque grows, it becomes unstable and may rupture. […] Due to the inflammatory milieu of the plaque, procoagulant factors are activated and fibrin production increases. […] While efferocytosis prevents inflammation and plaque growth, the impaired efferocytosis of apoptotic/necrotic bodies may lead to further deposition of macrophages/foam cells in the plaque. […] Due to the inflammatory conditions of the plaque, monocytes differentiate into DCs, which infiltrate the endothelium and release proinflammatory cytokines that promote inflammation and atherosclerosis. […] Stable plaques are featured by chronic low-grade inflammation, while unstable plaques exhibit active inflammation, which further promotes plaque rupture and vulnerability by thinning the fibrous cap.

• #50 PATHOGENESIS OF ATHEROSCLEROSIS – Histopathology.guru

  https://www.histopathology.guru/pathogenesis-of-atherosclerosis/

  Inflammation is triggered by accumulation of cholesterol crystals and free fatty acids in macrophages and other cells […] Activated macrophages produce reactive oxygen species that enhance LDL oxidation and elaborate growth factors that drive smooth muscle cell proliferation […] Intimal smooth muscle proliferation and extracellular matrix deposition convert fatty streak into a mature atheroma and contribute to progressive growth of atherosclerotic lesion.

• #51 Atherosclerosis: Process, Indicators, Risk Factors and New Hopes

  https://pmc.ncbi.nlm.nih.gov/articles/PMC4258672/

  Currently, atherosclerosis is a common disease in which fatty deposits called atheromatous plaques appear in the inner layers of arteries. […] Hyperlipidemia and hyperglycemia are related to increased oxidative damage, which affects antioxidant status and lipoprotein levels. […] Studies have shown that lipid lowering medicinal herbs can reduce the blood lipids especially after meals in addition to their antioxidant effects. […] The initial soft lesion is composed of foam cells and extracellular fat deposits and a small number of platelets. […] Severe damage to vascular tissue happens when adjacent SMC and endothelial cells secret small peptides such as cytokines and growth factors such as interleukin 1 (IL-1), and TNF (which causes cell growth). […] These processes weaken the formed plaque shaped fibrous cap and can destroy it.

• #52 Atherosclerosis: Process, Indicators, Risk Factors and New Hopes

  https://pmc.ncbi.nlm.nih.gov/articles/PMC4258672/

  The starting point of this process is the damage caused by combination of unsaturated lipids of plasma or arterial membrane with oxygen or side products of their oxidation. […] The produced aldehydes bond with amino groups of ApoB-100. […] Oxidation also converts phosphatidylcholine to lysophosphatidylcholine and produces sterols from cholesterol esters in lipid core of LDL. […] Nitric oxide is produced in the endothelium and rapidly leaks to reach to the molecular targets in the vascular walls and vascular channels. […] Nitric oxide has anti-atherogenic effects in addition to vascular tone adjustment capability. […] Inflammatory mechanisms have a pivotal role in all steps of atherosclerosis. […] C-reactive protein is a factor related to lipoprotein deposition and complement system activity in atherosclerotic plaques.

• #53 Inflammation in atherosclerosis: pathophysiology and mechanisms | Cell Death & Disease

  https://www.nature.com/articles/s41419-024-07166-8

  These findings corroborate the indispensable role of inflammation in the progression of atherosclerosis. […] One of the key events in atherogenesis is the cumulative oxidation of aggregated LDL within the plaque. […] The oxidation of LDL promotes its uptake by macrophages in the intimal layer. […] Hence, beyond the primary events, inflammation plays a decisive role in the exacerbation of the plaque and the progression of atherosclerosis. […] The hypoxia-induced activation of HIF-1 in macrophages may lead to the downregulation of PPAR-, thus driving plaque inflammation by reactivating proinflammatory genes and the repression of anti-inflammatory genes. […] Hypoxia activates the HIF-1 transcription factor in plaque macrophages, leading to the transactivation of proinflammatory genes such as cytokines (e.g. MIF).

• #54 Inflammation in atherosclerosis: pathophysiology and mechanisms | Cell Death & Disease

  https://www.nature.com/articles/s41419-024-07166-8

  These findings corroborate the indispensable role of inflammation in the progression of atherosclerosis. […] One of the key events in atherogenesis is the cumulative oxidation of aggregated LDL within the plaque. […] The oxidation of LDL promotes its uptake by macrophages in the intimal layer. […] Hence, beyond the primary events, inflammation plays a decisive role in the exacerbation of the plaque and the progression of atherosclerosis. […] The hypoxia-induced activation of HIF-1 in macrophages may lead to the downregulation of PPAR-, thus driving plaque inflammation by reactivating proinflammatory genes and the repression of anti-inflammatory genes. […] Hypoxia activates the HIF-1 transcription factor in plaque macrophages, leading to the transactivation of proinflammatory genes such as cytokines (e.g. MIF).

• #55 Inflammation in atherosclerosis: pathophysiology and mechanisms | Cell Death & Disease

  https://www.nature.com/articles/s41419-024-07166-8

  The binding and uptake of oxLDL by CD36 induce the activation of vimentin/FAK/NF-B axis in macrophages, resulting in cytokine release and inflammation. […] In summary, the described studies have shed light on the potential underlying mechanisms of macrophage-mediated inflammation after the exposure or uptake of oxLDL in atherosclerotic plaques.

• #56 EMAN RESEARCH PUBLISHING |Full Text|Platelet Implication in Atherosclerosis Pathogenesis

  https://www.publishing.emanresearch.org/Journal/FullText/5220

  Atherosclerosis is a prevalent cardiovascular disease that leads to serious complications like myocardial infarction and ischemic stroke. […] Platelets play a pivotal role in thrombosis and contribute to the development of atherosclerosis through interactions with the cellular environment. […] Consequently, platelets have emerged as a potential therapeutic target. […] This review explores the normal functioning of platelets and their involvement in atherosclerosis progression, highlighting their participation in inflammatory responses within the arterial wall. […] Platelets activate and release mediators that promote vascular inflammation and endothelial dysfunction, key features of atherosclerotic plaque formation. […] They also interact with circulating immune cells, exacerbating the inflammatory milieu and fostering disease progression.

• #57 EMAN RESEARCH PUBLISHING |Full Text|Platelet Implication in Atherosclerosis Pathogenesis

  https://www.publishing.emanresearch.org/Journal/FullText/5220

  Atherosclerosis is a prevalent cardiovascular disease that leads to serious complications like myocardial infarction and ischemic stroke. […] Platelets play a pivotal role in thrombosis and contribute to the development of atherosclerosis through interactions with the cellular environment. […] Consequently, platelets have emerged as a potential therapeutic target. […] This review explores the normal functioning of platelets and their involvement in atherosclerosis progression, highlighting their participation in inflammatory responses within the arterial wall. […] Platelets activate and release mediators that promote vascular inflammation and endothelial dysfunction, key features of atherosclerotic plaque formation. […] They also interact with circulating immune cells, exacerbating the inflammatory milieu and fostering disease progression.

• #58 Atherosclerotic cardiovascular disease – Knowledge @ AMBOSS

  https://www.amboss.com/us/knowledge/atherosclerotic-cardiovascular-disease/

  Atherosclerosis is a multifactorial inflammatory disease of the intima, manifesting at points of hemodynamic shear stress. […] The pathogenesis of atherosclerosis is precipitated by endothelial damage, which leads to inflammation and the formation of atheromas in vessel walls. […] Chronic stress on the endothelium (e.g., due to arterial hypertension and turbulence) leads to endothelial cell dysfunction, which results in the invasion of inflammatory cells (mainly monocytes and lymphocytes) through the disrupted endothelial barrier. […] Adhesion of platelets to the damaged vessel wall leads to platelet release of inflammatory mediators (e.g., cytokines) and platelet-derived growth factor (PDGF). […] PDGF stimulates the migration and proliferation of smooth muscle cells (SMCs) in the tunica intima and mediates the differentiation of fibroblasts into myofibroblasts.

• #59 Novel Insights into the Molecular Mechanisms of Atherosclerosis

  https://www.mdpi.com/1422-0067/24/17/13434

  Vitamin D signaling reduces the expression of TNFα, IL-6, IL-1, and IL-8 in isolated blood monocytes. […] MicroRNAs (miRNAs) are small non-coding RNAs that have diverse cellular roles but are best known for silencing and fine-tuning the expression of messenger RNA (mRNA) transcripts. […] These findings might shed new light on the cellular mechanisms of atherosclerosis and prospective targets for prevention and treatment in the future.

• #60

  https://www.cnic.es/en/noticias/circulation-new-mechanism-early-onset-atherosclerosis-premature-aging-syndrome

  The new study, published in the journal Circulation, opens a new avenue of research into treatments for the atherosclerosis associated with progeria. […] Scientists at the Centro Nacional de Investigaciones Cardiovasculares (CNIC) have identified the process of endothelial-to-mesenchymal transition (EndMT) as a novel mechanism in premature atherosclerosis in progeria. […] Atherosclerosis is characterized by the abnormal accumulation of cells and cholesterol in the arterial wall. […] The formation of atherosclerotic plaques progresses silently for many years and usually only begins to produce symptoms from mid-life. […] One of the most remarkable of these diseases is Hutchinson-Gilford progeria syndrome, also known as progeria, an extremely rare genetic disease characterized by premature aging during childhood and adolescence.

• #61

  https://www.cnic.es/en/noticias/circulation-new-mechanism-early-onset-atherosclerosis-premature-aging-syndrome

  This earlier work also demonstrated that one of the main causes of the accelerated atherosclerosis associated with this syndrome is the death of smooth muscle cells in the artery wall. […] Co-first author Dr. Rosa Nevado explained that in progeria, the loss of smooth muscle cells induces a series of pathological alterations in the neighboring endothelial cells. […] Dr. Andrs emphasized that the most startling change in endothelial cells from progeroid mice is the hyperactivation of phenotypic modulation via EndMT. […] This process consists of the loss of the typical features of endothelial cells and the acquisition of properties typical of mesenchymal cells that accelerate the development of atherosclerosis. […] The authors also conducted an in-depth analysis of the molecular mechanisms of EndMT in progeria. […] Dr. Hamczyk concluded, this study describes new cellular and molecular mechanisms involved in atherosclerosis and proposes a new therapeutic target for this disease.

• #62 Mechanism of Hypercholesterolemia-Induced Atherosclerosis

  https://www.imrpress.com/journal/RCM/23/6/10.31083/j.rcm2306212/htm

  Hypercholesterolemia is involved in the development of atherosclerosis and is a risk factor for coronary artery disease, stroke, and peripheral vascular disease. This paper deals with the mechanism of development of hypercholesterolemic atherosclerosis. Hypercholesterolemia increases the formation of numerous atherogenic biomolecules including reactive oxygen species (ROS), proinflammatory cytokines [interleukin (IL)-1, IL-2, IL-6, IL-8, tumor necrosis factor-alpha (TNF-α)], expression of intercellular adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule-1 (VCAM-1), E-selectin, monocyte chemoattractant protein-1 (MCP-1), granulocyte macrophage-colony stimulating factor (GM-CSF) and numerous growth factors [insulin-like growth factor-1 (IGF-1), platelet-derived growth factor-1 (PDGF-1) and transforming growth factor-beta (TGF-β)]. ROS mildly oxidizes low-density lipoprotein-cholesterol (LDL-C) to form minimally modified LDL (MM-LDL) which is further oxidized to form oxidized LDL (OX-LDL). Hypercholesterolemia also activates nuclear factor-kappa-B (NF-κB). The above atherogenic biomolecules are involved in the development of atherosclerosis which has been described in detail. Hypercholesterolemia also assists in the development of atherosclerosis through AGE (advanced glycation end-products)-RAGE (receptor for AGE) axis and C-reactive protein (CRP). Hypercholesterolemia is associated with increases in AGE, oxidative stress [AGE/sRAGE (soluble receptor for AGE)] and C-reactive protein, and decreases in the sRAGE, which are known to be implicated in the development of atherosclerosis. In conclusion, hypercholesterolemia induces atherosclerosis through increases in atherogenic biomolecules, AGE-RAGE axis and CRP.

• #63 Atherosclerosis: Process, Indicators, Risk Factors and New Hopes

  https://pmc.ncbi.nlm.nih.gov/articles/PMC4258672/

  The starting point of this process is the damage caused by combination of unsaturated lipids of plasma or arterial membrane with oxygen or side products of their oxidation. […] The produced aldehydes bond with amino groups of ApoB-100. […] Oxidation also converts phosphatidylcholine to lysophosphatidylcholine and produces sterols from cholesterol esters in lipid core of LDL. […] Nitric oxide is produced in the endothelium and rapidly leaks to reach to the molecular targets in the vascular walls and vascular channels. […] Nitric oxide has anti-atherogenic effects in addition to vascular tone adjustment capability. […] Inflammatory mechanisms have a pivotal role in all steps of atherosclerosis. […] C-reactive protein is a factor related to lipoprotein deposition and complement system activity in atherosclerotic plaques.

• #64 Atherosclerosis: Process, Indicators, Risk Factors and New Hopes

  https://pmc.ncbi.nlm.nih.gov/articles/PMC4258672/

  The humoral immune response might be a risk factor for coronary heart disease, inducing inflammation that links immunity with coronary disease. […] Atherosclerosis starts with fatty streaks formation and progresses with atheroma and atherosclerotic plaque formation. […] Lipid oxidation, in the form of Ox-LDL, demonstrates the first step of atherosclerosis.

• #65

  http://benthamscience.com/public/chapter/21850

  Atherosclerosis is characterized by hardening/narrowing of arteries and reduction of blood flow to vital organs. Animal models and human research show that endothelial dysfunction and plaque development precede the pathogenesis of atherosclerosis, and related coronary heart disease, neurological, and renal disorders. […] Biomarkers like C-reactive protein, IL-6, IL-8, phospholipase A2, cardiac troponin, MicroRNA, miR-21, and other endothelial inflammation biomarkers are novel targets for monitoring atherosclerosis-related cardiovascular disorders. […] New preventative measures and alternative therapies, including dietary interventions and plant-based foods may be the most cost-effective ways to manage atherosclerosis and cardiovascular illnesses.

• #66 Novel Insights into the Molecular Mechanisms of Atherosclerosis

  https://www.mdpi.com/1422-0067/24/17/13434

  The most crucial recommendations for the prevention of atherosclerosis include a proper diet, physical exercise, smoking cessation, adequate stress management, and good quality of sleep. […] Aging is one of the strongest risk factors for atherosclerosis which increases the morbidity and mortality of patients. Understanding the mechanisms of the age-related increase in atherosclerotic diseases can better guide prevention and therapy in this risk group. […] The vascular endothelium plays a regulatory role in vascular muscle contraction, relaxation, smooth muscle proliferation, and the expression of adhesion molecules or chemotactic factors. […] Endothelial dysfunction occurs under the influence of many factors, including local hemodynamic changes. […] Elevated serum UA is linked to various negative consequences, such as hypertension, chronic kidney diseases, and CVDs.

• #67 Novel Insights into the Molecular Mechanisms of Atherosclerosis

  https://www.mdpi.com/1422-0067/24/17/13434

  The most crucial recommendations for the prevention of atherosclerosis include a proper diet, physical exercise, smoking cessation, adequate stress management, and good quality of sleep. […] Aging is one of the strongest risk factors for atherosclerosis which increases the morbidity and mortality of patients. Understanding the mechanisms of the age-related increase in atherosclerotic diseases can better guide prevention and therapy in this risk group. […] The vascular endothelium plays a regulatory role in vascular muscle contraction, relaxation, smooth muscle proliferation, and the expression of adhesion molecules or chemotactic factors. […] Endothelial dysfunction occurs under the influence of many factors, including local hemodynamic changes. […] Elevated serum UA is linked to various negative consequences, such as hypertension, chronic kidney diseases, and CVDs.

• #68

  https://www.cnic.es/en/noticias/circulation-new-mechanism-early-onset-atherosclerosis-premature-aging-syndrome

  This earlier work also demonstrated that one of the main causes of the accelerated atherosclerosis associated with this syndrome is the death of smooth muscle cells in the artery wall. […] Co-first author Dr. Rosa Nevado explained that in progeria, the loss of smooth muscle cells induces a series of pathological alterations in the neighboring endothelial cells. […] Dr. Andrs emphasized that the most startling change in endothelial cells from progeroid mice is the hyperactivation of phenotypic modulation via EndMT. […] This process consists of the loss of the typical features of endothelial cells and the acquisition of properties typical of mesenchymal cells that accelerate the development of atherosclerosis. […] The authors also conducted an in-depth analysis of the molecular mechanisms of EndMT in progeria. […] Dr. Hamczyk concluded, this study describes new cellular and molecular mechanisms involved in atherosclerosis and proposes a new therapeutic target for this disease.

• #69 Atherosclerosis: current pathogenesis and therapeutic options | Nature Medicine

  https://www.nature.com/articles/nm.2538

  Coronary artery disease (CAD) arising from atherosclerosis is a leading cause of death and morbidity worldwide. The underlying pathogenesis involves an imbalanced lipid metabolism and a maladaptive immune response entailing a chronic inflammation of the arterial wall. […] The disturbed equilibrium of lipid accumulation, immune responses and their clearance is shaped by leukocyte trafficking and homeostasis governed by chemokines and their receptors. […] New pro- and anti-inflammatory pathways linking lipid and inflammation biology have been discovered, and genetic profiling studies have unveiled variations involved in human CAD. […] The growing understanding of the inflammatory processes and mediators has uncovered an intriguing diversity of targetable mechanisms that can be exploited to complement lipid-lowering therapies. […] Here we aim to systematically survey recently identified molecular mechanisms, translational developments and clinical strategies for targeting lipid-related inflammation in atherosclerosis and CAD.

• #70 Atherosclerosis: Process, Indicators, Risk Factors and New Hopes

  https://pmc.ncbi.nlm.nih.gov/articles/PMC4258672/

  Atherosclerosis is the major cause of morbidities and mortalities worldwide. […] Inflammation has a crucial role in pathogenesis of atherosclerosis. The disease is accompanied by excessive fibrosis of the intima, fatty plaques formation, proliferation of smooth muscle cells, and migration of a group of cells such as monocytes, T cells, and platelets which are formed in response to inflammation. […] The oxidation of low density lipoprotein (LDL) to Ox-LDL indicates the first step of atherosclerosis in cardiovascular diseases. […] The pathogenesis factors involved in atherosclerosis have recently been cleared and the discovery of these factors has brought about new hopes for better prevention and treatment of atherosclerosis. […] Atherosclerosis is the result of hyperlipidemia and lipid oxidation and has always been a major cause of mortality in developed countries.

• #71 What is the role of lipids in atherosclerosis and how low should we decrease lipid levels?

  https://www.escardio.org/Journals/E-Journal-of-Cardiology-Practice/Volume-18/what-is-the-role-of-lipids-in-atherosclerosis-and-how-low-should-we-decrease-lip

  Retention of apolipoprotein-B-containing lipoproteins within the arterial wall is the key initiating event in the pathobiology of atherosclerosis. […] Compelling evidence from preclinical investigations, Mendelian randomisation studies, epidemiologic observations, and randomised trials of lipid-modifying medications supports the key causal role of atherogenic lipoproteins, particularly low-density lipoprotein (LDL), in the pathogenesis of ASCVD. […] Importantly, dyslipidaemia is a modifiable risk factor, and pharmacologic LDL-cholesterol (LDL-C) lowering has been shown to halt the progression of atherosclerosis and improve clinical outcomes in the context of primary as well as secondary prevention. […] The totality of currently available evidence indicates that the greater the absolute reduction in plasma LDL-C levels, the larger the reduction of ASCVD risk, without offsetting safety issues arising from intensive lipid-lowering strategies.

• #72 EMAN RESEARCH PUBLISHING |Full Text|Platelet Implication in Atherosclerosis Pathogenesis

  https://www.publishing.emanresearch.org/Journal/FullText/5220

  Targeting platelets presents a promising approach for therapeutic interventions in atherosclerosis. […] Antiplatelet agents aim to impede platelet activation and aggregation, reducing thrombosis risk. […] Novel strategies that target platelet interactions with inflammatory cells and modulate platelet-derived inflammatory mediators are also being investigated. […] Further research is needed to fully exploit the potential of platelet-targeted therapy. […] Understanding the precise role of platelets at different stages of atherosclerosis and their interactions with immune cells and the inflammatory milieu will enhance our understanding of disease pathogenesis and guide the development of more effective therapeutic approaches. […] In conclusion, platelets significantly influence atherosclerosis by contributing to thrombus formation and promoting inflammatory processes. […] Recognizing platelets as a therapeutic target opens up new possibilities for mitigating the consequences of atherosclerosis and improving patient outcomes.

• #73 Efficacy and Mechanism of Alprostadil in Diabetes Mellitus Combined with Peripheral Atherosclerosis The Anatolian Journal of Cardiology

  https://anatoljcardiol.com/article/AJC-97421

  However, the therapeutic effects and mechanisms of Alprostadil in DM combined with peripheral atherosclerosis need to be further investigated. […] The aim of this study is to investigate the clinical adjuvant efficacy of Alprostadil in DM combined with peripheral atherosclerosis and its mechanism of action based on conventional drug therapy, so as to provide a reference basis for the clinical treatment of this disease. […] Alprostadil has also been reported to play a role in improving and protecting the kidney by inhibiting the immune response, reducing renal inflammation, and decreasing renal apoptosis. […] Alprostadil inhibits platelet aggregation and promotes platelet spreading. […] Alprostadil has ameliorative effects on HG- and ox-LDL-induced HUVECs. […] Alprostadil significantly inhibited HG- and ox-LDL-induced apoptosis in HUVECs.

• #74 Novel Insights into the Molecular Mechanisms of Atherosclerosis

  https://www.mdpi.com/1422-0067/24/17/13434

  The most crucial recommendations for the prevention of atherosclerosis include a proper diet, physical exercise, smoking cessation, adequate stress management, and good quality of sleep. […] Aging is one of the strongest risk factors for atherosclerosis which increases the morbidity and mortality of patients. Understanding the mechanisms of the age-related increase in atherosclerotic diseases can better guide prevention and therapy in this risk group. […] The vascular endothelium plays a regulatory role in vascular muscle contraction, relaxation, smooth muscle proliferation, and the expression of adhesion molecules or chemotactic factors. […] Endothelial dysfunction occurs under the influence of many factors, including local hemodynamic changes. […] Elevated serum UA is linked to various negative consequences, such as hypertension, chronic kidney diseases, and CVDs.

• #75

  http://benthamscience.com/public/chapter/21850

  Atherosclerosis is characterized by hardening/narrowing of arteries and reduction of blood flow to vital organs. Animal models and human research show that endothelial dysfunction and plaque development precede the pathogenesis of atherosclerosis, and related coronary heart disease, neurological, and renal disorders. […] Biomarkers like C-reactive protein, IL-6, IL-8, phospholipase A2, cardiac troponin, MicroRNA, miR-21, and other endothelial inflammation biomarkers are novel targets for monitoring atherosclerosis-related cardiovascular disorders. […] New preventative measures and alternative therapies, including dietary interventions and plant-based foods may be the most cost-effective ways to manage atherosclerosis and cardiovascular illnesses.

• #76 Cardiovascular disease

  https://www.nhs.uk/conditions/cardiovascular-disease/

  If you don’t exercise regularly, it’s more likely that you’ll have high blood pressure, high cholesterol levels and be overweight. All of these are risk factors for CVD. […] Being overweight or obese increases your risk of developing diabetes and high blood pressure, both of which are risk factors for CVD. […] If you have a family history of CVD, your risk of developing it is also increased. […] In the UK people of south Asian and Black African or African Caribbean background have an increased risk of getting CVD. […] A healthy lifestyle can lower your risk of CVD. If you already have CVD, staying as healthy as possible can reduce the chances of it getting worse.

• #77 Atherosclerosis: Symptoms, Causes & Treatment

  https://my.clevelandclinic.org/health/diseases/16753-atherosclerosis-arterial-disease

  Fatty streak formation. This is the first visible sign of atherosclerosis. […] Plaque growth. Dead foam cells and other debris keep building up, turning a fatty streak into a larger piece of plaque. […] Plaque rupture or erosion. In this stage, a blood clot forms in your artery due to plaque rupture or plaque erosion. […] Both events lead to the formation of a blood clot. The clot blocks blood flow and can lead to a heart attack or stroke. […] Atherosclerosis interferes with the normal workings of your cardiovascular system. […] It can limit or block blood flow to various parts of your body, including your heart and brain. […] Early diagnosis and treatment of atherosclerosis can help you avoid or delay complications.

• #78 Novel Insights into the Molecular Mechanisms of Atherosclerosis

  https://www.mdpi.com/1422-0067/24/17/13434

  Atherosclerosis is one of the most fatal diseases in the world. The associated thickening of the arterial wall and its background and consequences make it a very composite disease entity with many mechanisms that lead to its creation. […] This review summarizes the available information on the pathophysiological implications of atherosclerosis, focusing on endothelium dysfunction, inflammatory factors, aging, and uric acid, vitamin D, and miRNA expression as recent evidence of interactions of the molecular and cellular elements. Analyzing new discoveries for the underlying causes of this condition assists the general research to improve understanding of the mechanism of pathophysiology and thus prevention of cardiovascular diseases. […] The identification of atherogenesis as an active process rather than a passive cholesterol storage disease has highlighted important inflammatory, molecular, and cellular pathways.

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