Abstract
Atherosclerotic plaque vulnerability is a vital clinical problem as vulnerable plaques tend to rupture, which results in atherosclerosis complications—myocardial infarctions and subsequent cardiovascular deaths. Therefore, methods aiming to stabilize such plaques are in great demand. In this brief review, the idea of atherosclerotic plaque stabilization and five main approaches—towards the regulation of metabolism, macrophages and cellular death, inflammation, reactive oxygen species, and extracellular matrix remodeling have been presented. Moreover, apart from classical approaches (targeted at the general mechanisms of plaque destabilization), there are also alternative approaches targeted either at certain plaques which have just become vulnerable or targeted at the minimization of the consequences of atherosclerotic plaque erosion or rupture. These alternative approaches have also been briefly mentioned in this review.
Highlights
Atherosclerotic plaque is the pathophysiological basis of ischemic heart disease–a widespread disease in both developed and developing countries [1]
These processes change the microenvironment of the arterial wall intima, which promotes subsequent alterations—foam cell generation, vascular smooth muscle cell migration, and their conversion from contractile into the synthetic phenotype, extracellular matrix remodeling, plaque growth, fibrous cap formation, and necrotic core formation and calcifications [8,9]
According to the classic definition created by Virmani, vulnerable plaque is a thin-cap fibroatheroma (TCFA), characterized by a necrotic core presence with an
Summary
Atherosclerotic plaque is the pathophysiological basis of ischemic heart disease–a widespread disease in both developed and developing countries [1]. Local blood flow disturbances (nonlinear flow) in atherosclerosis-susceptible regions (e.g., arterial branches) cause decreased shear stress that is detected by the endothelial cells in the process of mechanotransduction These processes change the microenvironment of the arterial wall intima, which promotes subsequent alterations—foam cell generation, vascular smooth muscle cell migration, and their conversion from contractile into the synthetic phenotype, extracellular matrix remodeling, plaque growth, fibrous cap formation, and necrotic core formation and calcifications [8,9]. Hypoglycemic medications are supposed to be plaque-stabilizing and are antiatherosclerotic agents
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