Cellular and molecular mechanisms that underlies the formation of atherosclerotic plaque and plaque rupture-review

Atherosclerosis (AS) is the main risk factor for CVD and manifested by lipid accumulation, extracellular matrix protein deposition, and calcification in the intima and media of the large to medium size arteries promoting arterial stiffness and reduction of elasticity. It 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. This review focuses on the different stages of AS development, ranging from endothelial dysfunction to plaque rupture and the role of genetic abnormalities in AS development. In addition, the correlation of monocyte recruitment and atherogenesis, cytokine involvement with the role of phagocytosis in AS, fundamental signaling pathways in multiple stages of AS, and genetics of AS and the molecular mechanisms of plaque rupture and cap formation are covered here to provide a global view of the disease.