衰老
上睑下垂
坏死性下垂
程序性细胞死亡
氧化应激
炎症
自噬
细胞凋亡
内皮功能障碍
生物
细胞生物学
医学
内皮
免疫学
内科学
生物化学
作者
Lan-Lan Bu,Huanhuan Yuan,Liling Xie,Guofang Chen,Duan‐Fang Liao,Xi-Long Zheng
标识
DOI:10.3390/ijms242015160
摘要
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.
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