粒体自噬
线粒体
生物
发病机制
周围神经病变
外围设备
氧化应激
线粒体融合
细胞生物学
神经科学
线粒体DNA
自噬
免疫学
医学
遗传学
生物化学
内分泌学
内科学
基因
细胞凋亡
糖尿病
作者
Te Zhang,Jiannan Li,Guoqing Zhao
标识
DOI:10.1089/dna.2021.0529
摘要
Mitochondria provide energy for various cellular activities and are involved in the regulating of several physiological and pathological processes. Mitochondria constitute a dynamic network regulated by numerous quality control mechanisms; for example, division is necessary for mitochondria to develop, and fusion dilutes toxins produced by the mitochondria. Mitophagy removes damaged mitochondria. The etiologies of peripheral neuropathy include congenital and acquired diseases, and the pathogenesis varies; however, oxidative stress caused by mitochondrial damage is the accepted pathogenesis of peripheral neuropathy. Regulation and control of mitochondrial quality might point the way toward potential treatments for peripheral neuropathy. This article will review mitochondrial quality control mechanisms, their involvement in peripheral nerve diseases, and their potential therapeutic role.
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