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Cellular Senescence in Atherosclerosis: A Comprehensive Review of Mechanisms and Implications

Glory Coppe

Atherosclerosis, a chronic immune-inflammatory and age-related disorder characterized by lipid-rich plaques in arterial walls, remains the leading cause of global mortality. While advances in cardiology have improved our understanding of atherosclerosis, the underlying mechanisms continue to be complex. Recently, emerging evidence has shed light on the critical role of cellular senescence in this pathological process. Cellular senescence is characterized by irreversible cell cycle arrest and distinct phenotypic alterations, along with the production of senescence-associated secretory phenotype (SASP) factors, contributing to pro-inflammatory and pro-atherosclerotic responses. This review aims to provide an extensive examination of the current evidence regarding cellular senescence in atherosclerosis, focusing on its role in endothelial cells (ECs), vascular smooth muscle cells (VSMCs). We discuss the various causative stimuli for cellular senescence in atherosclerosis, including hyperlipidemia, hypertension, diabetes, obesity, DNA damage, oncogene signals, and mitochondrial dysfunction. Moreover, we explore the interplay between cellular senescence and atherosclerosis, emphasizing the involvement of senescent cells in the pathophysiological process. This comprehensive review aims to enhance our understanding of the molecular mechanisms underlying atherosclerosis and shed light on potential therapeutic strategies targeting cellular senescence for the prevention and treatment of this life-threatening disease.