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血管内皮细胞是沿血管腔表面排列的单层内皮细胞,将血管腔与血管平滑肌及组织分隔开,在维持血管稳态中具有重要的作用。心血管系统中复杂应激环境引起的内皮细胞整合应激反应(ISR)、炎症反应所造成的内皮细胞损伤是动脉粥样硬化的病因[1-2]。与肌组织细胞线粒体相比,内皮细胞线粒体的首要功能是参与信号转导维持细胞功能的完整,其次是进行能量代谢[3-4]。线粒体氧化应激是内皮细胞线粒体损伤的重要原因,而内皮细胞线粒体损伤引起细胞内信号转导异常和代谢紊乱,导致细胞的严重损伤[5]。本文重点阐述动脉粥样硬化病理进程中线粒体氧化应激引起内皮细胞损伤的作用及其机制。
Mitochondrial oxidative stress in vascular endothelial cell and atherosclerosis
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摘要: 血管内皮细胞损伤是动脉粥样硬化病理过程的起始环节。线粒体氧化应激与血管内皮细胞功能密切相关,线粒体氧化应激通过诱导线粒体自噬、一氧化氮生成减少、炎症反应、细胞代谢失衡和凋亡,导致血管内皮细胞的功能障碍。同时,血管内皮细胞也通过调控线粒体氧化应激维持自身稳态。本文旨在综述动脉粥样硬化病理过程中线粒体氧化应激诱发血管内皮细胞损伤的主要分子信号通路,为后续研究两者间的分子机制提供参考。Abstract: The injury of vascular endothelial cell function is the beginning of the pathological process of atherosclerosis. Mitochondrial oxidative stress is closely related to vascular endothelial cell function, which causes the dysfunction of vascular endothelial cell by inducing mitophagy, reducing nitric oxide production, inflammation, cellular metabolic imbalance and apoptosis. Meanwhile, vascular endothelial cell could also maintain their homeostasis by regulating mitochondrial oxidative stress. The molecular signaling pathways of the vascular endothelial cell injury caused by mitochondrial oxidative stress in the pathological process of atherosclerosis were outlined in this review, which provided reference for further research on the molecular mechanism between mitochondrial oxidative stress and endothelial damage.
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