粒体自噬
上睑下垂
细胞生物学
化学
内皮干细胞
细胞
自噬
细胞凋亡
程序性细胞死亡
生物
生物化学
体外
作者
Yanmei Chen,Yuan Chen,Wenjie Qing,Bo Yu,Dangheng Wei,Peng Wu
标识
DOI:10.1016/j.bbrc.2024.149667
摘要
Trimethylamine N-oxide (TMAO) is a novel risk factor for atherosclerosis, and its underlying regulatory mechanisms are under intensive investigation. Inflammation-related vascular endothelial damage is the major driver in atherogenic process. Pyroptosis, a type of proinflammatory programmed cell death, has been proved to promote the initiation and progression of atherosclerosis. In our study, we found that TMAO triggered endothelial cells excessive mitophagy, thereby facilitating pyroptosis. This process is mediated by the upexpression of phosphatidylethanolamine acyltransferase (LPEAT). These findings provide insights into TMAO-induced vascular endothelial cell damage and suggest that LPEAT may be a valuable target for the prevention and treatment of atherosclerosis.
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