Materiały źródłowe

• #1 Pathogenesis of coronary artery disease: focus on genetic risk factors and identification of genetic variants

  https://pmc.ncbi.nlm.nih.gov/articles/PMC3920464/

  Coronary artery disease (CAD) is the leading cause of death and disability worldwide, and its prevalence is expected to increase in the coming years. CAD events are caused by the interplay of genetic and environmental factors, the effects of which are mainly mediated through cardiovascular risk factors. […] CAD is a complex chronic inflammatory disease, characterized by remodeling and narrowing of the coronary arteries supplying oxygen to the heart. It can have various clinical manifestations, including stable angina, acute coronary syndrome, and sudden cardiac death. It has a complex etiopathogenesis and a multifactorial origin related to environmental factors, such as diet, smoking, and physical activity, and genetic factors that modulate risk of the disease both individually and through interaction.

• #2 Overview of Coronary Artery Disease – Cardiovascular Disorders – Merck Manual Professional Edition

  https://www.merckmanuals.com/professional/cardiovascular-disorders/coronary-artery-disease/overview-of-coronary-artery-disease

  Coronary artery disease is the leading cause of death in both sexes, accounting for approximately one third of all deaths, and substantial numbers of these occur in low resource areas. […] Usually, coronary artery disease is due to coronary artery atherosclerosis: Subintimal deposition of atheromas in large and medium-sized coronary arteries. […] Coronary atherosclerosis is often irregularly distributed in different vessels but typically occurs at points of turbulence (eg, vessel bifurcations). As the atheromatous plaque grows, the arterial lumen progressively narrows, resulting in ischemia (often causing angina pectoris). The degree of stenosis required to cause ischemia varies with oxygen demand. […] Occasionally, an atheromatous plaque ruptures or splits. Reasons are unclear but probably relate to plaque morphology, plaque calcium content, and plaque softening due to an inflammatory process. Rupture exposes collagen and other thrombogenic material, which activate platelets and the coagulation cascade, resulting in an acute thrombus, which interrupts coronary blood flow and causes some degree of myocardial ischemia.

• #3 Coronary Artery Disease – StatPearls – NCBI Bookshelf

  https://www.ncbi.nlm.nih.gov/books/NBK564304/

  Coronary artery disease (CAD) is characterized by the development of atherosclerosis in the coronary arteries, which can sometimes be asymptomatic. […] CAD is marked by an inadequate supply of blood and oxygen to the myocardium. The condition arises from occlusion of the coronary arteries and results in a demand-supply mismatch of oxygen. CAD typically involves the formation of plaques in the lumen of coronary arteries that impede blood flow. […] The hallmark of the pathophysiology of CAD is atherosclerotic plaque formation. Plaque is a buildup of fatty material that narrows the arterial lumen and impedes blood flow. The first step in the process is the formation of a „fatty streak” by subendothelial deposition of lipid-laden macrophages, also called „foam cells.” When a vascular insult occurs, the intima layer breaks, and monocytes migrate into the subendothelial space, where they become macrophages. These macrophages take up oxidized LDL particles, leading to foam cell formation. T cells get activated, and cytokines are released to aid in the inflammatory process. Growth factors activate smooth muscles, which also take up oxidized LDL particles and collagen, deposit along with activated macrophages, and increase the population of foam cells. Subendothelial plaque subsequently develops.

• #4 Pathogenesis of coronary artery disease: focus on genetic risk factors and identification of genetic variants

  https://pmc.ncbi.nlm.nih.gov/articles/PMC3920464/

  Atherosclerosis is the main etiopathogenic process that causes CAD, and its progression is related to an interplay between environmental and genetic factors, with the latter exerting their effects either directly or via cardiovascular risk factors. […] Briefly, atherosclerosis is a silent progressive chronic process characterized by accumulation of lipids, fibrous elements, and inflammatory molecules in the walls of the large arteries. This process begins with the efflux of low-density lipoprotein (LDL) cholesterol to the subendothelial space, which can then be modified and oxidized by various agents. […] The final result of this process is formation of the first typical atherosclerotic lesion, ie, the fatty streak, in which foam cells are present in the subendothelial space. […] The thickness of the fibrous cap is key for maintaining the integrity of the atherosclerotic plaque, and two types of plaque can be defined depending on the balance between formation and degradation of this fibrous cap, ie, stable and unstable or vulnerable.

• #5 Pathogenesis of coronary artery disease: focus on genetic risk factors and identification of genetic variants

  https://pmc.ncbi.nlm.nih.gov/articles/PMC3920464/

  Atherosclerosis is the main etiopathogenic process that causes CAD, and its progression is related to an interplay between environmental and genetic factors, with the latter exerting their effects either directly or via cardiovascular risk factors. […] Briefly, atherosclerosis is a silent progressive chronic process characterized by accumulation of lipids, fibrous elements, and inflammatory molecules in the walls of the large arteries. This process begins with the efflux of low-density lipoprotein (LDL) cholesterol to the subendothelial space, which can then be modified and oxidized by various agents. […] The final result of this process is formation of the first typical atherosclerotic lesion, ie, the fatty streak, in which foam cells are present in the subendothelial space. […] The thickness of the fibrous cap is key for maintaining the integrity of the atherosclerotic plaque, and two types of plaque can be defined depending on the balance between formation and degradation of this fibrous cap, ie, stable and unstable or vulnerable.

• #6 Azthena logo with the word Azthena

  https://www.news-medical.net/health/Coronary-Artery-Disease-Pathophysiology.aspx

  Coronary artery disease is usually caused by a build up cholesterol rich deposits or plaques on the lining inside the artery. These plaques are also called atheromatous plaques or simply atheromas and they cause a thickening of the arterial wall and a narrowing of the arterial space through which blood flows to reach the heart. The amount of blood reaching and supplying the heart muscles (myocardium) with oxygen and nutrients can therefore be reduced in the presence of atheromas. […] An atheroma usually starts to develop as a result of damage or injury to the inner lining of the artery called the endothelium. Once the endothelium is damaged, cholesterol, fats, lipoproteins and other debris start to accumulate at the site of injury in the wall or intima of the artery. […] High concentrations of low density lipoprotein (LDL) penetrate the damaged endothelium and undergo a chemical process called oxidation. This altered LDL acts as a beacon that attracts white blood cells or leukocytes to migrate towards the vessel wall. As macrophages appear, they engulf the lipoproteins and become foam cells. These foam cells give rise to the earliest visible form of an atheromatous lesion called the fatty streak.

• #7 Azthena logo with the word Azthena

  https://www.news-medical.net/health/Coronary-Artery-Disease-Pathophysiology.aspx

  Coronary artery disease is usually caused by a build up cholesterol rich deposits or plaques on the lining inside the artery. These plaques are also called atheromatous plaques or simply atheromas and they cause a thickening of the arterial wall and a narrowing of the arterial space through which blood flows to reach the heart. The amount of blood reaching and supplying the heart muscles (myocardium) with oxygen and nutrients can therefore be reduced in the presence of atheromas. […] An atheroma usually starts to develop as a result of damage or injury to the inner lining of the artery called the endothelium. Once the endothelium is damaged, cholesterol, fats, lipoproteins and other debris start to accumulate at the site of injury in the wall or intima of the artery. […] High concentrations of low density lipoprotein (LDL) penetrate the damaged endothelium and undergo a chemical process called oxidation. This altered LDL acts as a beacon that attracts white blood cells or leukocytes to migrate towards the vessel wall. As macrophages appear, they engulf the lipoproteins and become foam cells. These foam cells give rise to the earliest visible form of an atheromatous lesion called the fatty streak.

• #8 Coronary Artery Disease – StatPearls – NCBI Bookshelf

  https://www.ncbi.nlm.nih.gov/books/NBK564304/

  Coronary artery disease (CAD) is characterized by the development of atherosclerosis in the coronary arteries, which can sometimes be asymptomatic. […] CAD is marked by an inadequate supply of blood and oxygen to the myocardium. The condition arises from occlusion of the coronary arteries and results in a demand-supply mismatch of oxygen. CAD typically involves the formation of plaques in the lumen of coronary arteries that impede blood flow. […] The hallmark of the pathophysiology of CAD is atherosclerotic plaque formation. Plaque is a buildup of fatty material that narrows the arterial lumen and impedes blood flow. The first step in the process is the formation of a „fatty streak” by subendothelial deposition of lipid-laden macrophages, also called „foam cells.” When a vascular insult occurs, the intima layer breaks, and monocytes migrate into the subendothelial space, where they become macrophages. These macrophages take up oxidized LDL particles, leading to foam cell formation. T cells get activated, and cytokines are released to aid in the inflammatory process. Growth factors activate smooth muscles, which also take up oxidized LDL particles and collagen, deposit along with activated macrophages, and increase the population of foam cells. Subendothelial plaque subsequently develops.

• #9 Coronary Artery Disease – StatPearls – NCBI Bookshelf

  https://www.ncbi.nlm.nih.gov/books/NBK564304/

  Coronary artery disease (CAD) is characterized by the development of atherosclerosis in the coronary arteries, which can sometimes be asymptomatic. […] CAD is marked by an inadequate supply of blood and oxygen to the myocardium. The condition arises from occlusion of the coronary arteries and results in a demand-supply mismatch of oxygen. CAD typically involves the formation of plaques in the lumen of coronary arteries that impede blood flow. […] The hallmark of the pathophysiology of CAD is atherosclerotic plaque formation. Plaque is a buildup of fatty material that narrows the arterial lumen and impedes blood flow. The first step in the process is the formation of a „fatty streak” by subendothelial deposition of lipid-laden macrophages, also called „foam cells.” When a vascular insult occurs, the intima layer breaks, and monocytes migrate into the subendothelial space, where they become macrophages. These macrophages take up oxidized LDL particles, leading to foam cell formation. T cells get activated, and cytokines are released to aid in the inflammatory process. Growth factors activate smooth muscles, which also take up oxidized LDL particles and collagen, deposit along with activated macrophages, and increase the population of foam cells. Subendothelial plaque subsequently develops.

• #10 Coronary Artery Disease – StatPearls – NCBI Bookshelf

  https://www.ncbi.nlm.nih.gov/books/NBK564304/

  Coronary artery disease (CAD) is characterized by the development of atherosclerosis in the coronary arteries, which can sometimes be asymptomatic. […] CAD is marked by an inadequate supply of blood and oxygen to the myocardium. The condition arises from occlusion of the coronary arteries and results in a demand-supply mismatch of oxygen. CAD typically involves the formation of plaques in the lumen of coronary arteries that impede blood flow. […] The hallmark of the pathophysiology of CAD is atherosclerotic plaque formation. Plaque is a buildup of fatty material that narrows the arterial lumen and impedes blood flow. The first step in the process is the formation of a „fatty streak” by subendothelial deposition of lipid-laden macrophages, also called „foam cells.” When a vascular insult occurs, the intima layer breaks, and monocytes migrate into the subendothelial space, where they become macrophages. These macrophages take up oxidized LDL particles, leading to foam cell formation. T cells get activated, and cytokines are released to aid in the inflammatory process. Growth factors activate smooth muscles, which also take up oxidized LDL particles and collagen, deposit along with activated macrophages, and increase the population of foam cells. Subendothelial plaque subsequently develops.

• #11 Azthena logo with the word Azthena

  https://www.news-medical.net/health/Coronary-Artery-Disease-Pathophysiology.aspx

  Once the fatty streak is formed, it then attracts the smooth muscle cells to the site, where they multiply and start to produce extracellular matrix comprising of collagen and proteoglycan. It is this extracellular matrix that forms a large portion of the atherosclerotic plaque. This turns the fatty streak into a fibrous plaque. The lesion then starts to bulge into the inner wall of the blood vessel causing a significant narrowing of the luminal space. […] Next, the fibrous plaque starts to support itself. It develops its own small vessels to provide it with a supply of blood in a process called angiogenesis. Thereafter, the plaques begin to calcify as calcium starts to deposit. The final plaque is made up of a cap of fibrous tissue covering a core that is rich in lipids as well as necrotic or dead cells. The edge of this cap is key in acute coronary disease. This region is prone to rupture, which exposes the underlying core of lipids and necrotic material to thrombogenic factors in the blood. This can cause the aggregation of platelets that form a clot across the plaque and further narrow the artery.

• #12 Coronary Artery Disease – StatPearls – NCBI Bookshelf

  https://www.ncbi.nlm.nih.gov/books/NBK564304/

  The plaque could grow or become stable over time if no further endothelial insult occurs. A fibrous cap forms if the plaque becomes stable and the lesion calcifies over time. The lesion can become hemodynamically significant as time passes. Myocardial tissue perfusion can become insufficient, triggering angina symptoms during times of increased demand (eg, exercise) if the lumen has at least 70% obstruction. Symptoms often abate at rest as the oxygen requirement falls. Angina may occur at rest if the coronary artery is 90% stenosed. Some plaques can rupture and expose tissue factor, culminating in thrombosis that can cause subtotal or total occlusion of the lumen. Severe, acute obstruction typically results in ACS in the form of unstable angina, NSTEMI, or STEMI, depending on the level of insult.

• #13 Overview of Coronary Artery Disease – Cardiovascular Disorders – Merck Manual Professional Edition

  https://www.merckmanuals.com/professional/cardiovascular-disorders/coronary-artery-disease/overview-of-coronary-artery-disease

  Coronary artery disease is the leading cause of death in both sexes, accounting for approximately one third of all deaths, and substantial numbers of these occur in low resource areas. […] Usually, coronary artery disease is due to coronary artery atherosclerosis: Subintimal deposition of atheromas in large and medium-sized coronary arteries. […] Coronary atherosclerosis is often irregularly distributed in different vessels but typically occurs at points of turbulence (eg, vessel bifurcations). As the atheromatous plaque grows, the arterial lumen progressively narrows, resulting in ischemia (often causing angina pectoris). The degree of stenosis required to cause ischemia varies with oxygen demand. […] Occasionally, an atheromatous plaque ruptures or splits. Reasons are unclear but probably relate to plaque morphology, plaque calcium content, and plaque softening due to an inflammatory process. Rupture exposes collagen and other thrombogenic material, which activate platelets and the coagulation cascade, resulting in an acute thrombus, which interrupts coronary blood flow and causes some degree of myocardial ischemia.

• #14 Coronary Artery Disease – StatPearls – NCBI Bookshelf

  https://www.ncbi.nlm.nih.gov/books/NBK564304/

  Key stages involved in atherosclerotic plaque formation include the following. During atherosclerosis, vascular smooth muscle cells (SMCs) proliferate and migrate, forming a fibrous cap that stabilizes the plaque. These SMCs can undergo transdifferentiation, giving rise to various cell types within the plaque core, including osteoblast-like, myofibroblast-like, foam-like, and mesenchymal-stem-like cells. As SMCs release calcifying extracellular vesicles and undergo apoptosis, small calcified deposits, known as microcalcifications, form. […] Plaque stability is intimately linked with the type of calcification present. Stable plaques are often characterized by macrocalcifications and a thick, collagen-rich extracellular matrix within the fibrous cap, providing structural stability. In contrast, unstable plaques tend to have microcalcifications and a thin fibrous cap, heightening the risk of plaque rupture. Microcalcifications increase mechanical stress within the fibrous cap, making it more prone to rupture, potentially leading to myocardial infarction or stroke.

• #15 Coronary Artery Disease – StatPearls – NCBI Bookshelf

  https://www.ncbi.nlm.nih.gov/books/NBK564304/

  Key stages involved in atherosclerotic plaque formation include the following. During atherosclerosis, vascular smooth muscle cells (SMCs) proliferate and migrate, forming a fibrous cap that stabilizes the plaque. These SMCs can undergo transdifferentiation, giving rise to various cell types within the plaque core, including osteoblast-like, myofibroblast-like, foam-like, and mesenchymal-stem-like cells. As SMCs release calcifying extracellular vesicles and undergo apoptosis, small calcified deposits, known as microcalcifications, form. […] Plaque stability is intimately linked with the type of calcification present. Stable plaques are often characterized by macrocalcifications and a thick, collagen-rich extracellular matrix within the fibrous cap, providing structural stability. In contrast, unstable plaques tend to have microcalcifications and a thin fibrous cap, heightening the risk of plaque rupture. Microcalcifications increase mechanical stress within the fibrous cap, making it more prone to rupture, potentially leading to myocardial infarction or stroke.

• #16 Coronary Artery Disease – StatPearls – NCBI Bookshelf

  https://www.ncbi.nlm.nih.gov/books/NBK564304/

  The plaque could grow or become stable over time if no further endothelial insult occurs. A fibrous cap forms if the plaque becomes stable and the lesion calcifies over time. The lesion can become hemodynamically significant as time passes. Myocardial tissue perfusion can become insufficient, triggering angina symptoms during times of increased demand (eg, exercise) if the lumen has at least 70% obstruction. Symptoms often abate at rest as the oxygen requirement falls. Angina may occur at rest if the coronary artery is 90% stenosed. Some plaques can rupture and expose tissue factor, culminating in thrombosis that can cause subtotal or total occlusion of the lumen. Severe, acute obstruction typically results in ACS in the form of unstable angina, NSTEMI, or STEMI, depending on the level of insult.

• #17 Coronary Artery Disease – StatPearls – NCBI Bookshelf

  https://www.ncbi.nlm.nih.gov/books/NBK564304/

  The plaque could grow or become stable over time if no further endothelial insult occurs. A fibrous cap forms if the plaque becomes stable and the lesion calcifies over time. The lesion can become hemodynamically significant as time passes. Myocardial tissue perfusion can become insufficient, triggering angina symptoms during times of increased demand (eg, exercise) if the lumen has at least 70% obstruction. Symptoms often abate at rest as the oxygen requirement falls. Angina may occur at rest if the coronary artery is 90% stenosed. Some plaques can rupture and expose tissue factor, culminating in thrombosis that can cause subtotal or total occlusion of the lumen. Severe, acute obstruction typically results in ACS in the form of unstable angina, NSTEMI, or STEMI, depending on the level of insult.

• #18 Overview of Coronary Artery Disease – Cardiovascular Disorders – Merck Manual Professional Edition

  https://www.merckmanuals.com/professional/cardiovascular-disorders/coronary-artery-disease/overview-of-coronary-artery-disease

  Coronary artery disease is the leading cause of death in both sexes, accounting for approximately one third of all deaths, and substantial numbers of these occur in low resource areas. […] Usually, coronary artery disease is due to coronary artery atherosclerosis: Subintimal deposition of atheromas in large and medium-sized coronary arteries. […] Coronary atherosclerosis is often irregularly distributed in different vessels but typically occurs at points of turbulence (eg, vessel bifurcations). As the atheromatous plaque grows, the arterial lumen progressively narrows, resulting in ischemia (often causing angina pectoris). The degree of stenosis required to cause ischemia varies with oxygen demand. […] Occasionally, an atheromatous plaque ruptures or splits. Reasons are unclear but probably relate to plaque morphology, plaque calcium content, and plaque softening due to an inflammatory process. Rupture exposes collagen and other thrombogenic material, which activate platelets and the coagulation cascade, resulting in an acute thrombus, which interrupts coronary blood flow and causes some degree of myocardial ischemia.

• #19 Overview of Coronary Artery Disease – Cardiovascular Disorders – Merck Manual Professional Edition

  https://www.merckmanuals.com/professional/cardiovascular-disorders/coronary-artery-disease/overview-of-coronary-artery-disease

  Coronary artery disease is the leading cause of death in both sexes, accounting for approximately one third of all deaths, and substantial numbers of these occur in low resource areas. […] Usually, coronary artery disease is due to coronary artery atherosclerosis: Subintimal deposition of atheromas in large and medium-sized coronary arteries. […] Coronary atherosclerosis is often irregularly distributed in different vessels but typically occurs at points of turbulence (eg, vessel bifurcations). As the atheromatous plaque grows, the arterial lumen progressively narrows, resulting in ischemia (often causing angina pectoris). The degree of stenosis required to cause ischemia varies with oxygen demand. […] Occasionally, an atheromatous plaque ruptures or splits. Reasons are unclear but probably relate to plaque morphology, plaque calcium content, and plaque softening due to an inflammatory process. Rupture exposes collagen and other thrombogenic material, which activate platelets and the coagulation cascade, resulting in an acute thrombus, which interrupts coronary blood flow and causes some degree of myocardial ischemia.

• #20 Overview of Coronary Artery Disease – Cardiovascular Disorders – Merck Manual Professional Edition

  https://www.merckmanuals.com/professional/cardiovascular-disorders/coronary-artery-disease/overview-of-coronary-artery-disease

  The consequences of acute ischemia, collectively referred to as acute coronary syndromes (ACS), depend on the location and degree of obstruction and range from unstable angina, nonST-segment elevation myocardial infarction (NSTEMI), to ST-segment elevation myocardial infarction (STEMI), which can result in transmural infarction, and other complications including malignant ventricular arrhythmias, conduction defects, heart failure, and sudden death. […] Coronary artery spasm is a transient, focal increase in vascular tone, markedly narrowing the lumen and reducing blood flow; symptomatic ischemia (vasospastic angina) may result. […] In arteries with atheroma, the atheroma causes endothelial dysfunction, possibly resulting in local hypercontractility. Proposed mechanisms include loss of sensitivity to intrinsic vasodilators (eg, acetylcholine) and increased production of vasoconstrictors (eg, angiotensin II, endothelin, leukotrienes, serotonin, thromboxane) in the area of the atheroma. Recurrent spasm may damage the intima, leading to atheroma formation. […] Coronary artery dissection is a rare, non-traumatic tear in the coronary intima with creation of a false lumen. Blood flowing through the false lumen expands it, which restricts blood flow through the true lumen sometimes causing coronary ischemia or infarction.

• #21 Coronary artery disease in rheumatoid arthritis: Pathogenesis, risk factors, clinical manifestations, and diagnostic implications – UpToDate

  https://www.uptodate.com/contents/coronary-artery-disease-in-rheumatoid-arthritis-pathogenesis-risk-factors-clinical-manifestations-and-diagnostic-implications/print

  Coronary artery disease in rheumatoid arthritis: Pathogenesis, risk factors, clinical manifestations, and diagnostic implications […] The prevalence of atherosclerotic coronary artery disease (CAD) is increased in patients with chronic inflammatory diseases such as rheumatoid arthritis (RA) or systemic lupus erythematosus. […] The epidemiologic evidence, possible pathogenetic mechanisms, and clinical relevance of CAD in RA will be reviewed here. […] Many of the underlying mechanisms of pathogenesis of atherosclerosis are shared in patients with and without rheumatoid arthritis (RA). […] Among the general population, it is increasingly clear that inflammation has a significant role in the development of coronary artery disease (CAD) and that the innate and adaptive immune systems play an important role in the initiation and progression of atherosclerosis.

• #22 Vascular C-Reactive Protein in the Pathogenesis of Coronary Artery Disease:Role of Vascular Inflammation and Oxidative Stress

  https://eurekaselect.com/public/article/3220

  Atherosclerosis is considered to be a chronic inflammatory disease. Vascular inflammation occurs in response to injury induced by various stimuli, such as oxidative stress, shear stress, infection, and so on. […] This concept is supported by the recent clinical findings that C-reactive protein (CRP) is an independent risk factor for coronary heart disease. […] Recent investigations have provided two new concepts for the research field of CRP, namely, its extra-hepatic production and its potent biological activities such as the induction of adhesion molecules and chemokines. […] The expression of vascular CRP was closely associated with NAD(P)H oxidase, an important enzymatic origin of reactive oxygen species (ROS) in vessel walls. […] Furthermore, CRP directly up-regulated NAD(P)H oxidase p22phox and enhanced ROS generation in cultured coronary artery smooth muscle cells.

• #23 Pathophysiology of Cardiovascular Diseases: New Insights into Molecular Mechanisms of Atherosclerosis, Arterial Hypertension, and Coronary Artery Disease

  https://www.mdpi.com/2227-9059/10/8/1938

  Atherosclerosis occurs in these regions as a result of differences in flow, which is present at sites of low shear stress, turbulence, and oscillating flow. […] Endothelial dysfunction in modern cardiovascular medicine is described as changes in the production and availability of endothelial-derived NO, prostacyclin, and endothelin, as well as their impact on vascular reactivity. […] The vascular endothelium is the layer of cells lying under the epithelium lining the inside of the vessel and the muscular layer, which is a boundary between the circulating blood and the vascular wall. Its cells are specialized in maintaining vascular homeostasis, which is crucial for the proper functioning of organs, especially the heart. […] The endothelium is considered to be a strong indicator of cardiovascular function and fitness. Its dysfunction is considered to be the earliest marker of atherosclerosis and, in effect, CAD.

• #24 Pathophysiology of Cardiovascular Diseases: New Insights into Molecular Mechanisms of Atherosclerosis, Arterial Hypertension, and Coronary Artery Disease

  https://www.mdpi.com/2227-9059/10/8/1938

  Atherosclerosis occurs in these regions as a result of differences in flow, which is present at sites of low shear stress, turbulence, and oscillating flow. […] Endothelial dysfunction in modern cardiovascular medicine is described as changes in the production and availability of endothelial-derived NO, prostacyclin, and endothelin, as well as their impact on vascular reactivity. […] The vascular endothelium is the layer of cells lying under the epithelium lining the inside of the vessel and the muscular layer, which is a boundary between the circulating blood and the vascular wall. Its cells are specialized in maintaining vascular homeostasis, which is crucial for the proper functioning of organs, especially the heart. […] The endothelium is considered to be a strong indicator of cardiovascular function and fitness. Its dysfunction is considered to be the earliest marker of atherosclerosis and, in effect, CAD.

• #25 Vascular C-Reactive Protein in the Pathogenesis of Coronary Artery Disease:Role of Vascular Inflammation and Oxidative Stress

  https://eurekaselect.com/public/article/3220

  Atherosclerosis is considered to be a chronic inflammatory disease. Vascular inflammation occurs in response to injury induced by various stimuli, such as oxidative stress, shear stress, infection, and so on. […] This concept is supported by the recent clinical findings that C-reactive protein (CRP) is an independent risk factor for coronary heart disease. […] Recent investigations have provided two new concepts for the research field of CRP, namely, its extra-hepatic production and its potent biological activities such as the induction of adhesion molecules and chemokines. […] The expression of vascular CRP was closely associated with NAD(P)H oxidase, an important enzymatic origin of reactive oxygen species (ROS) in vessel walls. […] Furthermore, CRP directly up-regulated NAD(P)H oxidase p22phox and enhanced ROS generation in cultured coronary artery smooth muscle cells.

• #26 Vascular C-Reactive Protein in the Pathogenesis of Coronary Artery Disease:Role of Vascular Inflammation and Oxidative Stress

  https://eurekaselect.com/public/article/3220

  Atherosclerosis is considered to be a chronic inflammatory disease. Vascular inflammation occurs in response to injury induced by various stimuli, such as oxidative stress, shear stress, infection, and so on. […] This concept is supported by the recent clinical findings that C-reactive protein (CRP) is an independent risk factor for coronary heart disease. […] Recent investigations have provided two new concepts for the research field of CRP, namely, its extra-hepatic production and its potent biological activities such as the induction of adhesion molecules and chemokines. […] The expression of vascular CRP was closely associated with NAD(P)H oxidase, an important enzymatic origin of reactive oxygen species (ROS) in vessel walls. […] Furthermore, CRP directly up-regulated NAD(P)H oxidase p22phox and enhanced ROS generation in cultured coronary artery smooth muscle cells.

• #27 Vascular C-Reactive Protein in the Pathogenesis of Coronary Artery Disease:Role of Vascular Inflammation and Oxidative Stress

  https://eurekaselect.com/public/article/3220

  Atherosclerosis is considered to be a chronic inflammatory disease. Vascular inflammation occurs in response to injury induced by various stimuli, such as oxidative stress, shear stress, infection, and so on. […] This concept is supported by the recent clinical findings that C-reactive protein (CRP) is an independent risk factor for coronary heart disease. […] Recent investigations have provided two new concepts for the research field of CRP, namely, its extra-hepatic production and its potent biological activities such as the induction of adhesion molecules and chemokines. […] The expression of vascular CRP was closely associated with NAD(P)H oxidase, an important enzymatic origin of reactive oxygen species (ROS) in vessel walls. […] Furthermore, CRP directly up-regulated NAD(P)H oxidase p22phox and enhanced ROS generation in cultured coronary artery smooth muscle cells.

• #28 Vascular C-Reactive Protein in the Pathogenesis of Coronary Artery Disease:Role of Vascular Inflammation and Oxidative Stress

  https://eurekaselect.com/public/article/3220

  Atherosclerosis is considered to be a chronic inflammatory disease. Vascular inflammation occurs in response to injury induced by various stimuli, such as oxidative stress, shear stress, infection, and so on. […] This concept is supported by the recent clinical findings that C-reactive protein (CRP) is an independent risk factor for coronary heart disease. […] Recent investigations have provided two new concepts for the research field of CRP, namely, its extra-hepatic production and its potent biological activities such as the induction of adhesion molecules and chemokines. […] The expression of vascular CRP was closely associated with NAD(P)H oxidase, an important enzymatic origin of reactive oxygen species (ROS) in vessel walls. […] Furthermore, CRP directly up-regulated NAD(P)H oxidase p22phox and enhanced ROS generation in cultured coronary artery smooth muscle cells.

• #29 Vascular C-Reactive Protein in the Pathogenesis of Coronary Artery Disease:Role of Vascular Inflammation and Oxidative Stress

  https://eurekaselect.com/public/article/3220

  Thus, vascular CRP is likely to be a direct participant in vascular inflammation and lesion formation via its potent biological effects. […] Since lysophosphatidylcholine, a major atherogenic lipid of oxidized LDL, was reported to activate vascular NAD(P)H oxidase, we speculate that there is a vicious circle consisting of vascular NAD(P)H oxidase, ROS and oxidized LDL. […] In this review, we will discuss the roles of vascular CRP and NAD(P)H oxidase in the pathogenesis of CAD from the viewpoint of oxidative stress.

• #30

  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.

• #31

  https://crimsonpublishers.com/ojchd/fulltext/OJCHD.000545.php

  Coronary artery diseases (CAD) known as atherosclerotic heart disease, atherosclerotic cardiovascular disease, coronary heart disease (CHD), or ischemic heart disease (IHD). CAD is the largest contributor of cardiovascular diseases (CVDs) and mortality rate is due in prevalence to atherosclerosis, a chronic inflammatory condition of the arterial wall. Atherosclerosis is a pathological process that affects large- and medium-sized arteries and causes coronary artery disease (angina pectoris and myocardial infarction), cerebrovascular disease (ischemic stroke and vascular dementia) and peripheral vascular disease (intermittent claudication and gangrene). Atherosclerosis is a chronic cumulative disease progressing over years. It is characterized by atherosclerotic plaques formed in the wall of the vessels, consisting of necrotic cores, calcified regions, accumulated modified lipids, and inflamed smooth muscle cells (SMCs), endothelial cells, leukocytes, and foam cells. Lesions begin early as fatty streaks and progress into pathologic lesions under the influence of both genetic and lifestyle insults. The pathologist Felix Marchand first introduced the term atherosclerosis in 1904, describing the association of fatty degeneration and vessel stiffening. This process affects medium and large-sized arteries and is characterized by patchy intramural thickening of the sub-intima that encroaches on the arterial lumen. The earliest visible lesion of atherosclerosis is the fatty streak, which is due to an accumulation of lipid-laden foam cells in the intimal layer of the artery. With time; the fatty streak evolves into a fibrous plaque, the hallmark of established atherosclerosis. Ultimately the lesion may evolve to contain large amounts of lipid; if it becomes unstable, denudation of overlying endothelium, or plaque rupture, may result in thrombotic occlusion of the overlying artery. Atherosclerotic lesions (atheromata) are composed of three major components. The first is the cellular component comprised predominately of smooth muscle cells and macrophages. The second component is the connective tissue matrix and extracellular lipid. The third component is intracellular lipid that accumulates within macrophages, thereby converting them into foam cells. Atherosclerotic lesions develop as a result of inflammatory stimuli, subsequent release of various cytokines, proliferation of smooth muscle cells, synthesis of connective tissue matrix, and accumulation of macrophages and lipid. Excess generation of (ROS) represents an important pathological process in atherogenesis. Each component of the atherosclerotic blood vessel has been demonstrated to increase production of ROS, primarily superoxide anion. Important sources of ROS are vascular smooth muscle cells, endothelial cells, fibroblasts, and infiltrating leukocytes. Production of ROS affects gene transcription, damages DNA, and increases production of inflammatory transcription factors. The two best-characterized effects include oxidation of LDL and scavenging of endothelium-derived NO. The progression of atherosclerotic disease has been described as moving from an early lesion (phase1) to a more advanced fibro-lipid lesion (phase 2). The formation of thrombus or hematoma can advance into an acute phase (phase 3 and 4) or even to total occlusion (phase 5). Although there is substantial evidence for this process in the coronary circulation, it is highly likely that it also occurs in peripheral artery disease (PAD).

• #32

  https://crimsonpublishers.com/ojchd/fulltext/OJCHD.000545.php

  Coronary artery diseases (CAD) known as atherosclerotic heart disease, atherosclerotic cardiovascular disease, coronary heart disease (CHD), or ischemic heart disease (IHD). CAD is the largest contributor of cardiovascular diseases (CVDs) and mortality rate is due in prevalence to atherosclerosis, a chronic inflammatory condition of the arterial wall. Atherosclerosis is a pathological process that affects large- and medium-sized arteries and causes coronary artery disease (angina pectoris and myocardial infarction), cerebrovascular disease (ischemic stroke and vascular dementia) and peripheral vascular disease (intermittent claudication and gangrene). Atherosclerosis is a chronic cumulative disease progressing over years. It is characterized by atherosclerotic plaques formed in the wall of the vessels, consisting of necrotic cores, calcified regions, accumulated modified lipids, and inflamed smooth muscle cells (SMCs), endothelial cells, leukocytes, and foam cells. Lesions begin early as fatty streaks and progress into pathologic lesions under the influence of both genetic and lifestyle insults. The pathologist Felix Marchand first introduced the term atherosclerosis in 1904, describing the association of fatty degeneration and vessel stiffening. This process affects medium and large-sized arteries and is characterized by patchy intramural thickening of the sub-intima that encroaches on the arterial lumen. The earliest visible lesion of atherosclerosis is the fatty streak, which is due to an accumulation of lipid-laden foam cells in the intimal layer of the artery. With time; the fatty streak evolves into a fibrous plaque, the hallmark of established atherosclerosis. Ultimately the lesion may evolve to contain large amounts of lipid; if it becomes unstable, denudation of overlying endothelium, or plaque rupture, may result in thrombotic occlusion of the overlying artery. Atherosclerotic lesions (atheromata) are composed of three major components. The first is the cellular component comprised predominately of smooth muscle cells and macrophages. The second component is the connective tissue matrix and extracellular lipid. The third component is intracellular lipid that accumulates within macrophages, thereby converting them into foam cells. Atherosclerotic lesions develop as a result of inflammatory stimuli, subsequent release of various cytokines, proliferation of smooth muscle cells, synthesis of connective tissue matrix, and accumulation of macrophages and lipid. Excess generation of (ROS) represents an important pathological process in atherogenesis. Each component of the atherosclerotic blood vessel has been demonstrated to increase production of ROS, primarily superoxide anion. Important sources of ROS are vascular smooth muscle cells, endothelial cells, fibroblasts, and infiltrating leukocytes. Production of ROS affects gene transcription, damages DNA, and increases production of inflammatory transcription factors. The two best-characterized effects include oxidation of LDL and scavenging of endothelium-derived NO. The progression of atherosclerotic disease has been described as moving from an early lesion (phase1) to a more advanced fibro-lipid lesion (phase 2). The formation of thrombus or hematoma can advance into an acute phase (phase 3 and 4) or even to total occlusion (phase 5). Although there is substantial evidence for this process in the coronary circulation, it is highly likely that it also occurs in peripheral artery disease (PAD).

• #33 Pathophysiology of Cardiovascular Diseases: New Insights into Molecular Mechanisms of Atherosclerosis, Arterial Hypertension, and Coronary Artery Disease

  https://www.mdpi.com/2227-9059/10/8/1938

  Taking this into account, the endothelial dysfunction is directly related to a decreased production and sensitivity of cells to NO. As a result, we have an effective disturbance in the functioning of the entire vessel and its homeostasis, which leads to an observation of prothrombotic and proinflammatory phenomena, along with lower susceptibility of the blood vessel wall. […] Inflammation in diseases such as polyarteritis nodosa and cryoglobulinemia is driven by IC deposition (antibody-mediated IC formation, microaneurysms). […] In recent years, there has been substantial research showing correlations between genetic factors and endothelial function and dysfunction, which in turn are associated with an increased risk of developing CAD.

• #34 Pathogenesis of coronary artery disease: focus on genetic risk factors and identification of genetic variants

  https://pmc.ncbi.nlm.nih.gov/articles/PMC3920464/

  Our understanding of the genetic architecture of CAD has improved considerably since 2007 when the first GWAS of this disease were published. […] At the beginning of 2013, a meta-analysis of several GWAS identified a final set of about 40 genetic variants associated with CAD that explains approximately 6% of the heritability of CAD. […] Some of these variants are related to lipid metabolism, blood pressure, and inflammation, which confirms the importance of these pathways in the pathogenesis of CAD. […] The identification of genetic variants associated with disease has allowed us to improve our understanding of its pathogenesis, and ultimately to reduce the burden of disease at both the individual and population levels.

• #35 Pathogenesis of coronary artery disease: focus on genetic risk factors and identification of genetic variants

  https://pmc.ncbi.nlm.nih.gov/articles/PMC3920464/

  Our understanding of the genetic architecture of CAD has improved considerably since 2007 when the first GWAS of this disease were published. […] At the beginning of 2013, a meta-analysis of several GWAS identified a final set of about 40 genetic variants associated with CAD that explains approximately 6% of the heritability of CAD. […] Some of these variants are related to lipid metabolism, blood pressure, and inflammation, which confirms the importance of these pathways in the pathogenesis of CAD. […] The identification of genetic variants associated with disease has allowed us to improve our understanding of its pathogenesis, and ultimately to reduce the burden of disease at both the individual and population levels.

• #36 Pathogenesis of coronary artery disease: focus on genetic risk factors and identification of genetic variants

  https://pmc.ncbi.nlm.nih.gov/articles/PMC3920464/

  Our understanding of the genetic architecture of CAD has improved considerably since 2007 when the first GWAS of this disease were published. […] At the beginning of 2013, a meta-analysis of several GWAS identified a final set of about 40 genetic variants associated with CAD that explains approximately 6% of the heritability of CAD. […] Some of these variants are related to lipid metabolism, blood pressure, and inflammation, which confirms the importance of these pathways in the pathogenesis of CAD. […] The identification of genetic variants associated with disease has allowed us to improve our understanding of its pathogenesis, and ultimately to reduce the burden of disease at both the individual and population levels.

• #37 Role of LncRNAs in the Pathogenesis of Coronary Artery Disease

  https://www.imrpress.com/journal/RCM/24/4/10.31083/j.rcm2404096

  Coronary artery disease (CAD), caused by coronary artery occlusion, is a common cardiovascular disease worldwide. Long non-coding RNAs (lncRNAs) are implicated in the regulation of endothelial cell injury, angiogenesis, plaque formation, and other pathological mechanisms in CAD by acting on different cell types. Some lncRNAs are significantly upregulated in CAD patients; however, other lncRNAs are significantly downregulated. Differential expression of lncRNAs in CAD patients enables them to be exploited as potential biomarkers to evaluate disease progression and diagnosis/prognosis in CAD patients. In this study, we reviewed the role of lncRNAs in the development of different clinical subtypes of CAD.

• #38 Role of LncRNAs in the Pathogenesis of Coronary Artery Disease

  https://www.imrpress.com/journal/RCM/24/4/10.31083/j.rcm2404096

  Coronary artery disease (CAD), caused by coronary artery occlusion, is a common cardiovascular disease worldwide. Long non-coding RNAs (lncRNAs) are implicated in the regulation of endothelial cell injury, angiogenesis, plaque formation, and other pathological mechanisms in CAD by acting on different cell types. Some lncRNAs are significantly upregulated in CAD patients; however, other lncRNAs are significantly downregulated. Differential expression of lncRNAs in CAD patients enables them to be exploited as potential biomarkers to evaluate disease progression and diagnosis/prognosis in CAD patients. In this study, we reviewed the role of lncRNAs in the development of different clinical subtypes of CAD.

• #39 Circular RNAs in coronary heart disease: From molecular mechanism to promising clinical application (Review)

  https://www.spandidos-publications.com/10.3892/ijmm.2024.5452

  CircRNAs participate in regulating endothelial cell function in CHD through complex molecular mechanisms involving the sponging of miRNAs and subsequent modulation of mRNA targets. […] CircRNAs have a vital role in the inflammatory response associated with the development of CHD. […] Therefore, circRNAs mediate the inflammatory response in CHD by regulating miRNA and mRNA interactions, influencing cell proliferation, oxidative stress and atherosclerosis, thereby contributing to disease development and progression. […] Dysregulated circRNAs have been implicated in the phenotypes and function of VSMCs during CHD progression. […] Hence, circRNAs boost CHD progression by facilitating VSMC proliferation and differentiation. […] Thus, the integration of circRNAs into the therapeutic landscape of CHD represents a promising frontier, with ongoing research aimed at optimizing these strategies for clinical application.

• #40 Circular RNAs in coronary heart disease: From molecular mechanism to promising clinical application (Review)

  https://www.spandidos-publications.com/10.3892/ijmm.2024.5452

  CircRNAs participate in regulating endothelial cell function in CHD through complex molecular mechanisms involving the sponging of miRNAs and subsequent modulation of mRNA targets. […] CircRNAs have a vital role in the inflammatory response associated with the development of CHD. […] Therefore, circRNAs mediate the inflammatory response in CHD by regulating miRNA and mRNA interactions, influencing cell proliferation, oxidative stress and atherosclerosis, thereby contributing to disease development and progression. […] Dysregulated circRNAs have been implicated in the phenotypes and function of VSMCs during CHD progression. […] Hence, circRNAs boost CHD progression by facilitating VSMC proliferation and differentiation. […] Thus, the integration of circRNAs into the therapeutic landscape of CHD represents a promising frontier, with ongoing research aimed at optimizing these strategies for clinical application.

• #41 Circular RNAs in coronary heart disease: From molecular mechanism to promising clinical application (Review)

  https://www.spandidos-publications.com/10.3892/ijmm.2024.5452

  CircRNAs participate in regulating endothelial cell function in CHD through complex molecular mechanisms involving the sponging of miRNAs and subsequent modulation of mRNA targets. […] CircRNAs have a vital role in the inflammatory response associated with the development of CHD. […] Therefore, circRNAs mediate the inflammatory response in CHD by regulating miRNA and mRNA interactions, influencing cell proliferation, oxidative stress and atherosclerosis, thereby contributing to disease development and progression. […] Dysregulated circRNAs have been implicated in the phenotypes and function of VSMCs during CHD progression. […] Hence, circRNAs boost CHD progression by facilitating VSMC proliferation and differentiation. […] Thus, the integration of circRNAs into the therapeutic landscape of CHD represents a promising frontier, with ongoing research aimed at optimizing these strategies for clinical application.

• #42 Circular RNAs in coronary heart disease: From molecular mechanism to promising clinical application (Review)

  https://www.spandidos-publications.com/10.3892/ijmm.2024.5452

  CircRNAs participate in regulating endothelial cell function in CHD through complex molecular mechanisms involving the sponging of miRNAs and subsequent modulation of mRNA targets. […] CircRNAs have a vital role in the inflammatory response associated with the development of CHD. […] Therefore, circRNAs mediate the inflammatory response in CHD by regulating miRNA and mRNA interactions, influencing cell proliferation, oxidative stress and atherosclerosis, thereby contributing to disease development and progression. […] Dysregulated circRNAs have been implicated in the phenotypes and function of VSMCs during CHD progression. […] Hence, circRNAs boost CHD progression by facilitating VSMC proliferation and differentiation. […] Thus, the integration of circRNAs into the therapeutic landscape of CHD represents a promising frontier, with ongoing research aimed at optimizing these strategies for clinical application.

• #43 Molecular mechanisms of coronary artery disease risk at the PDGFD locus | Nature Communications

  https://www.nature.com/articles/s41467-023-36518-9

  Genome wide association studies for coronary artery disease (CAD) have identified a risk locus at 11q22.3. Here, we verify with mechanistic studies that rs2019090 and PDGFD represent the functional variant and gene at this locus. […] These findings suggest that PDGFD mediates CAD risk by promoting deleterious phenotypic changes in SMC, along with an inflammatory response that is primarily focused in the adventitia. […] Recent GWAS meta-analyses have identified approximately 250 loci that confer CAD risk. […] While atherosclerosis has been characterized as a primarily inflammatory disease, there has been a dearth of such molecules linked to the disease process by human GWAS studies. […] The locus encoding PDGFD has been identified in GWAS studies to be associated with CAD risk. […] Here, through fine mapping approaches we present data suggesting that PDGFD is the disease gene for CAD at this locus and further provide evidence to support the mechanism of association to be due to FOXC1/C2 differential binding at the rs2019090 associated variant.

• #44 Molecular mechanisms of coronary artery disease risk at the PDGFD locus | Nature Communications

  https://www.nature.com/articles/s41467-023-36518-9

  Genome wide association studies for coronary artery disease (CAD) have identified a risk locus at 11q22.3. Here, we verify with mechanistic studies that rs2019090 and PDGFD represent the functional variant and gene at this locus. […] These findings suggest that PDGFD mediates CAD risk by promoting deleterious phenotypic changes in SMC, along with an inflammatory response that is primarily focused in the adventitia. […] Recent GWAS meta-analyses have identified approximately 250 loci that confer CAD risk. […] While atherosclerosis has been characterized as a primarily inflammatory disease, there has been a dearth of such molecules linked to the disease process by human GWAS studies. […] The locus encoding PDGFD has been identified in GWAS studies to be associated with CAD risk. […] Here, through fine mapping approaches we present data suggesting that PDGFD is the disease gene for CAD at this locus and further provide evidence to support the mechanism of association to be due to FOXC1/C2 differential binding at the rs2019090 associated variant.

• #45 Molecular mechanisms of coronary artery disease risk at the PDGFD locus | Nature Communications

  https://www.nature.com/articles/s41467-023-36518-9

  Together, we provide evidence that supports PDGFD as the disease gene at this CAD risk locus and reveal insights into its role in mediating vascular smooth muscle specific phenotypic changes and plaque biology. […] Pdgfd promotes SMC phenotypic transitions as well as monocyte-macrophage recruitment. […] Together, these data indicate that loss of Pdgfd inhibits SMC phenotypic transition and monocyte-macrophage recruitment during atherosclerosis development. […] Taken together, these results support the scRNAseq findings and suggest two prominent mechanisms by which Pdgfd expression may promote disease risk. Pdgfd was found to promote de-differentiation of SMC, their migration into the plaque, and transition to the CMC phenotype, which we have correlated to disease risk. […] Taken together these data suggest that Pdgfd contributes a substantial portion but not all of the migratory effect of Pdgf signaling, which is likely mediated through the Pdgfrb receptor.

• #46 Molecular mechanisms of coronary artery disease risk at the PDGFD locus | Nature Communications

  https://www.nature.com/articles/s41467-023-36518-9

  Together, we provide evidence that supports PDGFD as the disease gene at this CAD risk locus and reveal insights into its role in mediating vascular smooth muscle specific phenotypic changes and plaque biology. […] Pdgfd promotes SMC phenotypic transitions as well as monocyte-macrophage recruitment. […] Together, these data indicate that loss of Pdgfd inhibits SMC phenotypic transition and monocyte-macrophage recruitment during atherosclerosis development. […] Taken together, these results support the scRNAseq findings and suggest two prominent mechanisms by which Pdgfd expression may promote disease risk. Pdgfd was found to promote de-differentiation of SMC, their migration into the plaque, and transition to the CMC phenotype, which we have correlated to disease risk. […] Taken together these data suggest that Pdgfd contributes a substantial portion but not all of the migratory effect of Pdgf signaling, which is likely mediated through the Pdgfrb receptor.

• #47 Molecular mechanisms of coronary artery disease risk at the PDGFD locus | Nature Communications

  https://www.nature.com/articles/s41467-023-36518-9

  Despite these striking changes in vascular SMC phenotype, neither our studies of Pdgfd or the recent study of Pdgfrb showed a substantial effect on plaque burden in knockout mice for these two genes. […] We propose that PDGFD is an important contributor to the inflammatory cell milieu in the plaque, and that this mechanism accounts at least in part for its contribution to CAD risk.

• #48 Molecular mechanisms of coronary artery disease risk at the PDGFD locus | Nature Communications

  https://www.nature.com/articles/s41467-023-36518-9

  Despite these striking changes in vascular SMC phenotype, neither our studies of Pdgfd or the recent study of Pdgfrb showed a substantial effect on plaque burden in knockout mice for these two genes. […] We propose that PDGFD is an important contributor to the inflammatory cell milieu in the plaque, and that this mechanism accounts at least in part for its contribution to CAD risk.

• #49 Pathogenesis, Assessment, and Treatment of Coronary Microcirculation Dysfunction – ABC Cardiol

  https://abccardiol.org/en/article/pathogenesis-assessment-and-treatment-of-coronary-microcirculation-dysfunction/

  Cardiovascular disease is the predominant cause of mortality on a global scale. […] Research indicates that women exhibit a greater likelihood of presenting with non-obstructive coronary artery disease (CAD) when experiencing symptoms of myocardial ischemia in comparison to men. […] Additionally, women tend to experience a higher burden of symptoms relative to men, and despite the presence of ischemic heart disease, they are frequently reassured erroneously due to the absence of obstructive CAD. […] In cases of ischemic heart disease accompanied by symptoms of myocardial ischemia but lacking obstructive CAD, it is imperative to consider coronary microvascular dysfunction as a potential underlying cause. […] Coronary microvascular dysfunction, characterized by impaired coronary flow reserve resulting from functional and/or structural abnormalities in the microcirculation, is linked to adverse cardiovascular outcomes.

• #50 Pathogenesis, Assessment, and Treatment of Coronary Microcirculation Dysfunction – ABC Cardiol

  https://abccardiol.org/en/article/pathogenesis-assessment-and-treatment-of-coronary-microcirculation-dysfunction/

  Cardiovascular disease is the predominant cause of mortality on a global scale. […] Research indicates that women exhibit a greater likelihood of presenting with non-obstructive coronary artery disease (CAD) when experiencing symptoms of myocardial ischemia in comparison to men. […] Additionally, women tend to experience a higher burden of symptoms relative to men, and despite the presence of ischemic heart disease, they are frequently reassured erroneously due to the absence of obstructive CAD. […] In cases of ischemic heart disease accompanied by symptoms of myocardial ischemia but lacking obstructive CAD, it is imperative to consider coronary microvascular dysfunction as a potential underlying cause. […] Coronary microvascular dysfunction, characterized by impaired coronary flow reserve resulting from functional and/or structural abnormalities in the microcirculation, is linked to adverse cardiovascular outcomes.

• #51 Pathogenesis, Assessment, and Treatment of Coronary Microcirculation Dysfunction – ABC Cardiol

  https://abccardiol.org/en/article/pathogenesis-assessment-and-treatment-of-coronary-microcirculation-dysfunction/

  Cardiovascular disease is the predominant cause of mortality on a global scale. […] Research indicates that women exhibit a greater likelihood of presenting with non-obstructive coronary artery disease (CAD) when experiencing symptoms of myocardial ischemia in comparison to men. […] Additionally, women tend to experience a higher burden of symptoms relative to men, and despite the presence of ischemic heart disease, they are frequently reassured erroneously due to the absence of obstructive CAD. […] In cases of ischemic heart disease accompanied by symptoms of myocardial ischemia but lacking obstructive CAD, it is imperative to consider coronary microvascular dysfunction as a potential underlying cause. […] Coronary microvascular dysfunction, characterized by impaired coronary flow reserve resulting from functional and/or structural abnormalities in the microcirculation, is linked to adverse cardiovascular outcomes.

• #52 Pathogenesis, Assessment, and Treatment of Coronary Microcirculation Dysfunction – ABC Cardiol

  https://abccardiol.org/en/article/pathogenesis-assessment-and-treatment-of-coronary-microcirculation-dysfunction/

  Lifestyle modifications and the use of anti-atherosclerotic and anti-anginal medications may offer potential benefits, although further clinical trials are necessary to inform treatment strategies. […] This review aims to explore the prevalence, underlying mechanisms, diagnostic approaches, and therapeutic interventions for coronary microvascular dysfunction.

• #53 Coronary artery disease in rheumatoid arthritis: Pathogenesis, risk factors, clinical manifestations, and diagnostic implications – UpToDate

  https://www.uptodate.com/contents/coronary-artery-disease-in-rheumatoid-arthritis-pathogenesis-risk-factors-clinical-manifestations-and-diagnostic-implications/print

  Coronary artery disease in rheumatoid arthritis: Pathogenesis, risk factors, clinical manifestations, and diagnostic implications […] The prevalence of atherosclerotic coronary artery disease (CAD) is increased in patients with chronic inflammatory diseases such as rheumatoid arthritis (RA) or systemic lupus erythematosus. […] The epidemiologic evidence, possible pathogenetic mechanisms, and clinical relevance of CAD in RA will be reviewed here. […] Many of the underlying mechanisms of pathogenesis of atherosclerosis are shared in patients with and without rheumatoid arthritis (RA). […] Among the general population, it is increasingly clear that inflammation has a significant role in the development of coronary artery disease (CAD) and that the innate and adaptive immune systems play an important role in the initiation and progression of atherosclerosis.

• #54 Coronary artery disease in rheumatoid arthritis: Pathogenesis, risk factors, clinical manifestations, and diagnostic implications – UpToDate

  https://www.uptodate.com/contents/coronary-artery-disease-in-rheumatoid-arthritis-pathogenesis-risk-factors-clinical-manifestations-and-diagnostic-implications/print

  Coronary artery disease in rheumatoid arthritis: Pathogenesis, risk factors, clinical manifestations, and diagnostic implications […] The prevalence of atherosclerotic coronary artery disease (CAD) is increased in patients with chronic inflammatory diseases such as rheumatoid arthritis (RA) or systemic lupus erythematosus. […] The epidemiologic evidence, possible pathogenetic mechanisms, and clinical relevance of CAD in RA will be reviewed here. […] Many of the underlying mechanisms of pathogenesis of atherosclerosis are shared in patients with and without rheumatoid arthritis (RA). […] Among the general population, it is increasingly clear that inflammation has a significant role in the development of coronary artery disease (CAD) and that the innate and adaptive immune systems play an important role in the initiation and progression of atherosclerosis.

• #55 Identification of the susceptible genes and mechanism underlying the comorbid presence of coronary artery disease and rheumatoid arthritis: a network modularization analysis | BMC Genomics | Full Text

  https://bmcgenomics.biomedcentral.com/articles/10.1186/s12864-023-09519-7

  The comorbidities of coronary artery disease (CAD) and rheumatoid arthritis (RA) are mutual risk factors, which lead to higher mortality, but the biological mechanisms connecting the two remain unclear. […] The underlying mechanisms of CAD-associated progression of RA are not fully elucidated. Studies found that the high mortality of CADRA is due to endothelial dysfunction and the circulating acute phase reactants such as C-reactive proteins. […] Inflammation can promote coronary atherosclerosis and induce coronary microvascular dysfunction in patients with RA, leading to an inadequate supply of myocardial oxygen, with the primary incipient procedures for the two changes being endothelial dysfunction and immune system dysregulation. […] Neutrophil activation-related genes of S100A8 and S100A12 are under investigation as therapeutic targets for both RA and CAD, hinting at the common pathogenic mechanisms of CADRA.

• #56 Identification of the susceptible genes and mechanism underlying the comorbid presence of coronary artery disease and rheumatoid arthritis: a network modularization analysis | BMC Genomics | Full Text

  https://bmcgenomics.biomedcentral.com/articles/10.1186/s12864-023-09519-7

  The comorbidities of coronary artery disease (CAD) and rheumatoid arthritis (RA) are mutual risk factors, which lead to higher mortality, but the biological mechanisms connecting the two remain unclear. […] The underlying mechanisms of CAD-associated progression of RA are not fully elucidated. Studies found that the high mortality of CADRA is due to endothelial dysfunction and the circulating acute phase reactants such as C-reactive proteins. […] Inflammation can promote coronary atherosclerosis and induce coronary microvascular dysfunction in patients with RA, leading to an inadequate supply of myocardial oxygen, with the primary incipient procedures for the two changes being endothelial dysfunction and immune system dysregulation. […] Neutrophil activation-related genes of S100A8 and S100A12 are under investigation as therapeutic targets for both RA and CAD, hinting at the common pathogenic mechanisms of CADRA.

• #57 Identification of the susceptible genes and mechanism underlying the comorbid presence of coronary artery disease and rheumatoid arthritis: a network modularization analysis | BMC Genomics | Full Text

  https://bmcgenomics.biomedcentral.com/articles/10.1186/s12864-023-09519-7

  The comorbidities of coronary artery disease (CAD) and rheumatoid arthritis (RA) are mutual risk factors, which lead to higher mortality, but the biological mechanisms connecting the two remain unclear. […] The underlying mechanisms of CAD-associated progression of RA are not fully elucidated. Studies found that the high mortality of CADRA is due to endothelial dysfunction and the circulating acute phase reactants such as C-reactive proteins. […] Inflammation can promote coronary atherosclerosis and induce coronary microvascular dysfunction in patients with RA, leading to an inadequate supply of myocardial oxygen, with the primary incipient procedures for the two changes being endothelial dysfunction and immune system dysregulation. […] Neutrophil activation-related genes of S100A8 and S100A12 are under investigation as therapeutic targets for both RA and CAD, hinting at the common pathogenic mechanisms of CADRA.

• #58 Identification of the susceptible genes and mechanism underlying the comorbid presence of coronary artery disease and rheumatoid arthritis: a network modularization analysis | BMC Genomics | Full Text

  https://bmcgenomics.biomedcentral.com/articles/10.1186/s12864-023-09519-7

  The comorbidities of coronary artery disease (CAD) and rheumatoid arthritis (RA) are mutual risk factors, which lead to higher mortality, but the biological mechanisms connecting the two remain unclear. […] The underlying mechanisms of CAD-associated progression of RA are not fully elucidated. Studies found that the high mortality of CADRA is due to endothelial dysfunction and the circulating acute phase reactants such as C-reactive proteins. […] Inflammation can promote coronary atherosclerosis and induce coronary microvascular dysfunction in patients with RA, leading to an inadequate supply of myocardial oxygen, with the primary incipient procedures for the two changes being endothelial dysfunction and immune system dysregulation. […] Neutrophil activation-related genes of S100A8 and S100A12 are under investigation as therapeutic targets for both RA and CAD, hinting at the common pathogenic mechanisms of CADRA.

• #59

  https://www.jci.org/articles/view/108350/scanned-page/1079

  Homocystinuria, an abnormality of methionine metabolism is associated with severe vascular disease in infancy and childhood. […] Methionine metabolism was investigated in 25 patients aged under 50 with angiographically proved coronary artery disease and in 22 control patients, of whom 17 had normal coronary arteries at angiography and 5 were healthy volunteers. […] These results suggest a reduced ability to metabolise homocysteine in some patients with premature coronary artery disease when this pathway is stressed.

• #60

  https://www.jci.org/articles/view/108350/scanned-page/1079

  Homocystinuria, an abnormality of methionine metabolism is associated with severe vascular disease in infancy and childhood. […] Methionine metabolism was investigated in 25 patients aged under 50 with angiographically proved coronary artery disease and in 22 control patients, of whom 17 had normal coronary arteries at angiography and 5 were healthy volunteers. […] These results suggest a reduced ability to metabolise homocysteine in some patients with premature coronary artery disease when this pathway is stressed.

• #61

  https://www.jci.org/articles/view/108350/scanned-page/1079

  Homocystinuria, an abnormality of methionine metabolism is associated with severe vascular disease in infancy and childhood. […] Methionine metabolism was investigated in 25 patients aged under 50 with angiographically proved coronary artery disease and in 22 control patients, of whom 17 had normal coronary arteries at angiography and 5 were healthy volunteers. […] These results suggest a reduced ability to metabolise homocysteine in some patients with premature coronary artery disease when this pathway is stressed.

• #62 Mechanism of HMGB1–RAGE in Kawasaki disease with coronary artery injury | European Journal of Medical Research | Full Text

  https://eurjmedres.biomedcentral.com/articles/10.1186/s40001-020-00406-5

  Kawasaki disease (KD) is a common, yet unknown etiology disease in Asian countries, which causes acquired heart disease in childhood. It is characterized by an inflammatory acute febrile vasculitis of medium-sized arteries, particularly the coronary arteries. […] The purpose of our study was to verify the mechanism and clinical significance of HMGB1-RAGE in coronary artery injury of Kawasaki disease. […] The findings of this study demonstrate that the expression of HMGB1/RAGE/NF-B is altered at different stages of KD, suggesting that the HMGB1/RAGE/NF-B signaling pathway plays an important role in vascular injury in KD. […] The incidence of coronary artery lesions (CALs) is 2530% in children without regular treatment, while it will be reduced to 5% with the correct treatment during the early period.

• #63 Mechanism of HMGB1–RAGE in Kawasaki disease with coronary artery injury | European Journal of Medical Research | Full Text

  https://eurjmedres.biomedcentral.com/articles/10.1186/s40001-020-00406-5

  Kawasaki disease (KD) is a common, yet unknown etiology disease in Asian countries, which causes acquired heart disease in childhood. It is characterized by an inflammatory acute febrile vasculitis of medium-sized arteries, particularly the coronary arteries. […] The purpose of our study was to verify the mechanism and clinical significance of HMGB1-RAGE in coronary artery injury of Kawasaki disease. […] The findings of this study demonstrate that the expression of HMGB1/RAGE/NF-B is altered at different stages of KD, suggesting that the HMGB1/RAGE/NF-B signaling pathway plays an important role in vascular injury in KD. […] The incidence of coronary artery lesions (CALs) is 2530% in children without regular treatment, while it will be reduced to 5% with the correct treatment during the early period.

• #64 Mechanism of HMGB1–RAGE in Kawasaki disease with coronary artery injury | European Journal of Medical Research | Full Text

  https://eurjmedres.biomedcentral.com/articles/10.1186/s40001-020-00406-5

  The pathological changes are similar to those of infant nodular polyarteritis, with arterial full-thickness inflammation, intimal thickening, granulocyte and monocyte infiltration, internal elastic layer and medial membrane rupture, vascular wall necrosis, and aneurysm formation. […] The receptor for advanced glycation end products (RAGE) is a high-affinity receptor of HMGB1 currently known, while not the only receptor for HMGB1. […] The binding of HMGB1 to RAGE promotes the activation of mitogen, and the phosphorylation of protein kinases (such as p38 kinase, SAPK/JNK, and ERK1/2), and subsequently activates various signaling pathways, such as NF-B and MAPKp38, inducing the production of inflammatory cytokines and chemokines. […] The serum levels of HMGB1 have been shown to be significantly increased in the acute phase of KD.

• #65 Mechanism of HMGB1–RAGE in Kawasaki disease with coronary artery injury | European Journal of Medical Research | Full Text

  https://eurjmedres.biomedcentral.com/articles/10.1186/s40001-020-00406-5

  The pathological changes are similar to those of infant nodular polyarteritis, with arterial full-thickness inflammation, intimal thickening, granulocyte and monocyte infiltration, internal elastic layer and medial membrane rupture, vascular wall necrosis, and aneurysm formation. […] The receptor for advanced glycation end products (RAGE) is a high-affinity receptor of HMGB1 currently known, while not the only receptor for HMGB1. […] The binding of HMGB1 to RAGE promotes the activation of mitogen, and the phosphorylation of protein kinases (such as p38 kinase, SAPK/JNK, and ERK1/2), and subsequently activates various signaling pathways, such as NF-B and MAPKp38, inducing the production of inflammatory cytokines and chemokines. […] The serum levels of HMGB1 have been shown to be significantly increased in the acute phase of KD.

• #66 Mechanism of HMGB1–RAGE in Kawasaki disease with coronary artery injury | European Journal of Medical Research | Full Text

  https://eurjmedres.biomedcentral.com/articles/10.1186/s40001-020-00406-5

  The pathological changes are similar to those of infant nodular polyarteritis, with arterial full-thickness inflammation, intimal thickening, granulocyte and monocyte infiltration, internal elastic layer and medial membrane rupture, vascular wall necrosis, and aneurysm formation. […] The receptor for advanced glycation end products (RAGE) is a high-affinity receptor of HMGB1 currently known, while not the only receptor for HMGB1. […] The binding of HMGB1 to RAGE promotes the activation of mitogen, and the phosphorylation of protein kinases (such as p38 kinase, SAPK/JNK, and ERK1/2), and subsequently activates various signaling pathways, such as NF-B and MAPKp38, inducing the production of inflammatory cytokines and chemokines. […] The serum levels of HMGB1 have been shown to be significantly increased in the acute phase of KD.

• #67 Mechanism of HMGB1–RAGE in Kawasaki disease with coronary artery injury | European Journal of Medical Research | Full Text

  https://eurjmedres.biomedcentral.com/articles/10.1186/s40001-020-00406-5

  In summary, we hypothesized that HMGB1-RAGE may be associated with the development of KD; particularly, in the acute phase when HMGB1 accumulates in coronary endothelial cells, causing coronary vasculitis and promoting coronary artery dilatation. […] The findings of this study indicate that the expression of HMGB1, RAGE, and NF-B were significantly increased in the acute phase of children with KD, which was of great value for the early diagnosis of KD, and the expression of HMGB1, RAGE, and NF-B in CAL group were significantly higher than that in NCAL group, which indicate that it is involved in the occurrence and development of KD coronary injury.

• #68 Mechanism of HMGB1–RAGE in Kawasaki disease with coronary artery injury | European Journal of Medical Research | Full Text

  https://eurjmedres.biomedcentral.com/articles/10.1186/s40001-020-00406-5

  In summary, we hypothesized that HMGB1-RAGE may be associated with the development of KD; particularly, in the acute phase when HMGB1 accumulates in coronary endothelial cells, causing coronary vasculitis and promoting coronary artery dilatation. […] The findings of this study indicate that the expression of HMGB1, RAGE, and NF-B were significantly increased in the acute phase of children with KD, which was of great value for the early diagnosis of KD, and the expression of HMGB1, RAGE, and NF-B in CAL group were significantly higher than that in NCAL group, which indicate that it is involved in the occurrence and development of KD coronary injury.

• #69 Researchers identify 12 cell types associated with the pathogenesis of coronary artery disease

  https://medicalxpress.com/news/2023-04-cell-pathogenesis-coronary-artery-disease.html

  Researchers identify 12 cell types associated with the pathogenesis of coronary artery disease. A new study from the University of Eastern Finland identified 12 different cell types involved in the pathogenesis of coronary artery disease, CAD. The researchers also showed that the genetic risk factors for CAD take their effect especially via smooth vascular muscle cells, which change their phenotype as the disease progresses. […] According to Professor Kaikkonen-Määtä, the findings significantly increase our understanding of the pathogenesis of coronary artery disease: „The way the disease progresses in different people may, in part, be affected by different genetic risk factors that are mediated via different cell types and mechanisms. This understanding may help to prevent the disease more effectively in the future, while also enabling the development of better and individually tailored treatments,” she says. […] Coronary artery disease is a major public health concern globally, which can lead to heart attack and stroke as the disease progresses. Coronary artery disease is one of the leading causes of death worldwide.

• #70 Researchers identify 12 cell types associated with the pathogenesis of coronary artery disease

  https://medicalxpress.com/news/2023-04-cell-pathogenesis-coronary-artery-disease.html

  Researchers identify 12 cell types associated with the pathogenesis of coronary artery disease. A new study from the University of Eastern Finland identified 12 different cell types involved in the pathogenesis of coronary artery disease, CAD. The researchers also showed that the genetic risk factors for CAD take their effect especially via smooth vascular muscle cells, which change their phenotype as the disease progresses. […] According to Professor Kaikkonen-Määtä, the findings significantly increase our understanding of the pathogenesis of coronary artery disease: „The way the disease progresses in different people may, in part, be affected by different genetic risk factors that are mediated via different cell types and mechanisms. This understanding may help to prevent the disease more effectively in the future, while also enabling the development of better and individually tailored treatments,” she says. […] Coronary artery disease is a major public health concern globally, which can lead to heart attack and stroke as the disease progresses. Coronary artery disease is one of the leading causes of death worldwide.

• #71 How a cholesterol drug may prevent heart attacks

  https://medicalxpress.com/news/2025-05-cholesterol-drug-heart.html

  A new study conducted at Cedars-Sinai reveals how the cholesterol-reducing drug evolocumab prevents heart attacks in people with coronary artery disease—a leading cause of death in the United States. […] Coronary artery disease occurs when cholesterol deposits build up in the walls of the heart’s arteries, leading to formation of plaques that begin as areas of inflammation. When inflamed plaques grow large, they become prone to rupture, which can cause heart attack. […] „Our findings demonstrate that reducing inflammation may be an important mechanism for reducing the risk of heart attack with these powerful drugs.”

• #72 How a cholesterol drug may prevent heart attacks

  https://medicalxpress.com/news/2025-05-cholesterol-drug-heart.html

  A new study conducted at Cedars-Sinai reveals how the cholesterol-reducing drug evolocumab prevents heart attacks in people with coronary artery disease—a leading cause of death in the United States. […] Coronary artery disease occurs when cholesterol deposits build up in the walls of the heart’s arteries, leading to formation of plaques that begin as areas of inflammation. When inflamed plaques grow large, they become prone to rupture, which can cause heart attack. […] „Our findings demonstrate that reducing inflammation may be an important mechanism for reducing the risk of heart attack with these powerful drugs.”

• #73 Identification of the susceptible genes and mechanism underlying the comorbid presence of coronary artery disease and rheumatoid arthritis: a network modularization analysis | BMC Genomics | Full Text

  https://bmcgenomics.biomedcentral.com/articles/10.1186/s12864-023-09519-7

  A total of 14 GO function terms were enriched by the differentiated modules, the top three terms were cAMP-dependent protein kinase activity, demethylase activity, and regulation of calcium ion import. […] Among the identified hub genes, several were reportedly related to CAD or RA. A study demonstrated that the IL19 risk allele was relevant to stroke/MI in SLE and RA, but not in the general population, showing that shared immune pathways may be contained in cardiovascular disease pathogenesis and inflammatory rheumatic diseases. […] The expression levels of cell adhesion molecules increased in patients with RA, and were associated with disease activity, oxidative stress, and inflammatory markers targeting the expression of these molecules is an important therapeutic strategy for RA. […] Although we have found several of the related modules and susceptible genes, certain limitations for our study also exist. For limited datasets and samples involving the comorbidities, CAD and RA, cross validation could not be performed.

• #74 Pathogenesis of coronary artery disease: focus on genetic risk factors and identification of genetic variants

  https://pmc.ncbi.nlm.nih.gov/articles/PMC3920464/

  Our understanding of the genetic architecture of CAD has improved considerably since 2007 when the first GWAS of this disease were published. […] At the beginning of 2013, a meta-analysis of several GWAS identified a final set of about 40 genetic variants associated with CAD that explains approximately 6% of the heritability of CAD. […] Some of these variants are related to lipid metabolism, blood pressure, and inflammation, which confirms the importance of these pathways in the pathogenesis of CAD. […] The identification of genetic variants associated with disease has allowed us to improve our understanding of its pathogenesis, and ultimately to reduce the burden of disease at both the individual and population levels.

• #75 Pathophysiology of Cardiovascular Diseases: New Insights into Molecular Mechanisms of Atherosclerosis, Arterial Hypertension, and Coronary Artery Disease

  https://www.mdpi.com/2227-9059/10/8/1938

  Taking this into account, the endothelial dysfunction is directly related to a decreased production and sensitivity of cells to NO. As a result, we have an effective disturbance in the functioning of the entire vessel and its homeostasis, which leads to an observation of prothrombotic and proinflammatory phenomena, along with lower susceptibility of the blood vessel wall. […] Inflammation in diseases such as polyarteritis nodosa and cryoglobulinemia is driven by IC deposition (antibody-mediated IC formation, microaneurysms). […] In recent years, there has been substantial research showing correlations between genetic factors and endothelial function and dysfunction, which in turn are associated with an increased risk of developing CAD.

• #76 Vascular C-Reactive Protein in the Pathogenesis of Coronary Artery Disease:Role of Vascular Inflammation and Oxidative Stress

  https://eurekaselect.com/public/article/3220

  Atherosclerosis is considered to be a chronic inflammatory disease. Vascular inflammation occurs in response to injury induced by various stimuli, such as oxidative stress, shear stress, infection, and so on. […] This concept is supported by the recent clinical findings that C-reactive protein (CRP) is an independent risk factor for coronary heart disease. […] Recent investigations have provided two new concepts for the research field of CRP, namely, its extra-hepatic production and its potent biological activities such as the induction of adhesion molecules and chemokines. […] The expression of vascular CRP was closely associated with NAD(P)H oxidase, an important enzymatic origin of reactive oxygen species (ROS) in vessel walls. […] Furthermore, CRP directly up-regulated NAD(P)H oxidase p22phox and enhanced ROS generation in cultured coronary artery smooth muscle cells.

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