New Dawn for Atherosclerosis: Vascular Endothelial Cell Senescence and Death

• Published in: International journal of molecular sciences Vol. 24; no. 20; p. 15160
• Main Authors: Bu, Lan-Lan, Yuan, Huan-Huan, Xie, Ling-Li, Guo, Min-Hua, Liao, Duan-Fang, Zheng, Xi-Long
• Format: Journal Article
• Language: English
• Published: Switzerland MDPI AG 13.10.2023; MDPI
• Subjects: Adhesion; Adhesives; Aging; Apoptosis; Atherosclerosis; Atherosclerosis - metabolism; B cells; Biomechanics; Cardiovascular disease; Cell cycle; Cellular Senescence - physiology; Collagen; Development and progression; Endothelial Cells - metabolism; Endothelium; Fibroblasts; Genotype & phenotype; Humans; Hypertension; Inflammation; Kinases; Leukocytes; Metabolism; Metabolites; Morphology; Oxidative Stress; Pathogenesis; Review; Sapropterin dihydrochloride; Senescence; Signal Transduction; Spectrum analysis; Veins & arteries; atherosclerosis; endothelial cell death; endothelial cell; endothelial cell senescence
• ISSN: 1422-0067; 1661-6596; 1422-0067
• DOI: 10.3390/ijms242015160

Endothelial cells (ECs) form the inner linings of blood vessels, and are directly exposed to endogenous hazard signals and metabolites in the circulatory system. The senescence and death of ECs are not only adverse outcomes, but also causal contributors to endothelial dysfunction, an early risk marker of atherosclerosis. The pathophysiological process of EC senescence involves both structural and functional changes and has been linked to various factors, including oxidative stress, dysregulated cell cycle, hyperuricemia, vascular inflammation, and aberrant metabolite sensing and signaling. Multiple forms of EC death have been documented in atherosclerosis, including autophagic cell death, apoptosis, pyroptosis, NETosis, necroptosis, and ferroptosis. Despite this, the molecular mechanisms underlying EC senescence or death in atherogenesis are not fully understood. To provide a comprehensive update on the subject, this review examines the historic and latest findings on the molecular mechanisms and functional alterations associated with EC senescence and death in different stages of atherosclerosis.