Vascular smooth muscle cells (VSMC) migrate and proliferate to form a stabilizing fibrous cap that encapsulates atherosclerotic plaques. Several studies demonstrated that the vascular smooth muscle cells have phenotypes that differ in the media and atherosclerotic lesions, and that phenotypic switching of SMCs plays a central role in atherosclerosis according to Ross's hypothesis [3, 4].It has been proposed that before migration from the media into the intima, a transition of the … p53, an essential molecule in cell cycle and apoptosis control, also plays a central role in atherosclerosis. The historical view of vascular smooth muscle cells (VSMCs) in atherosclerosis is that aberrant proliferation of VSMCs promotes plaque formation, but that VSMCs in advanced plaques are entirely beneficial, for example preventing rupture of the fibrous cap. Introduction. Atherosclerosis and the arterial smooth muscle cell: Proliferation of smooth muscle is a key event in the genesis of the lesions of atherosclerosis. Atherosclerosis is the leading cause of death and disability. Abstract: The historical view of vascular smooth muscle cells (VSMCs) in atherosclerosis is that aberrant proliferation of VSMCs promotes plaque formation, but that VSMCs in advanced plaques are entirely beneficial, for example preventing rupture of the fibrous cap. Introduction. Excessive vascular smooth muscle cell (VSMC) proliferation contributes to the development of atherosclerosis and restenosis. Science. However, this view has been based on ideas that there is a … Furthermore, apoptosis of VSMCs accelerates plaque rupture in the atherosclerotic vessels. Phenotypic switching. 1. 1973 Jun 29;180(4093):1332-9. However, this view has been based on ideas … Invasion of medial vascular smooth muscle cells from media to intima and proliferation of vascular smooth muscle cells in the intima together contribute to plaque formation. 1 Vascular smooth muscle cells (VSMCs) play indispensable roles during the development of atherosclerosis, such as proliferation, migration, apoptosis and autophagy. Sirtuin 6 (SIRT6) is a nuclear deacetylase involved in DNA damage response signaling, inflammation and metabolism; however, its role in regulating VSMC senescence and atherosclerosis … 1 – 3 Inactivation of p53 stimulates the development of atherosclerosis. The excessive proliferation and migration of abnormal vascular smooth muscle cells (VSMCs) are the major causes of atherogenesis [1].Recent studies have shown that enhanced glycolysis is involved in platelet-derived growth factor-induced VSMC proliferation and migration [2, 3].Furthermore, increased glycolytic flux is critical for the bioenergetic shift that … Vascular smooth muscle cell (VSMC) accumulation is a hallmark of atherosclerosis, 1 and VSMCs also generate the bulk of the neointima formed after vessel occlusion or injury. 2.1. During the advanced stage of atherosclerosis, vascular smooth muscle cells play a beneficial role in plaque stabilization. CD98 is a transmembrane protein made of two subunits, CD98 heavy chain (CD98hc) and one of six light chains, and is known to be involved in cell proliferation and survival. Proliferation of vascular smooth muscle cells (VSMCs) and the formation of neointima dominate atherosclerotic lesion development. 2 – 4 VSMCs display remarkable phenotypic plasticity in vitro, 5 and lineage-tracing experiments have convincingly shown that VSMC phenotypic switching occurs in vivo. Rationale: Vascular smooth muscle cell (VSMC) senescence promotes atherosclerosis and features of plaque instability, in part through lipid-mediated oxidative DNA damage and telomere dysfunction. Atherosclerosis, a chronic inflammatory arterial disease, is associated with dyslipidemia or dyslipoproteinemia and changes in the structural of the blood vessel wall. The historical view of vascular smooth muscle cells (VSMCs) in atherosclerosis is that aberrant proliferation of VSMCs promotes plaque formation, but that VSMCs in advanced plaques are entirely beneficial, for example preventing rupture of the fibrous cap.