Pathogenesis of Atherosclerosis: Review
Journal of Pharmaceutical Research International · pp. 54–62 · Published 11 Jul 2022
10.9734/jpri/2022/v34i44A36334Abstract
In atherosclerosis, apolipoprotein B-lipoproteins in blood artery matrix attract monocytes, which become macrophages and dendritic cells. Macrophages generated from recruited monocytes cause a maladaptive, non-resolving inflammatory response that increases subendothelial layer. Some lesions cause myocardial infarction, stroke, and sudden cardiac death. Modern atherosclerosis research focuses on the molecular biology of atherogenesis, although the disease's complex pathophysiology is still unknown. The goal of this research is to examine the mechanisms of atherosclerosis development, such as endothelial dysfunction, fatty streak formation, fibrous plaque formation, and plaque rupture (Fig. 1.). This article takes a thorough look at the pathophysiology of atherosclerosis, addressing the pathological and biochemical mechanisms of atherosclerotic plaque development and growth. Atherosclerosis pathogenesis and disease development are the primary topics of discussion in this review, which focuses on the disease's particular targets.
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