粒体自噬
生物
先天免疫系统
自噬
线粒体
品脱1
炎症体
细胞生物学
炎症
线粒体融合
干扰素基因刺激剂
免疫
干扰素
免疫系统
线粒体DNA
免疫学
神经科学
基因
遗传学
细胞凋亡
作者
Andrew T. Moehlman,Richard J. Youle
标识
DOI:10.1146/annurev-cellbio-021820-101354
摘要
Maintaining mitochondrial health is essential for the survival and function of eukaryotic organisms. Misfunctioning mitochondria activate stress-responsive pathways to restore mitochondrial network homeostasis, remove damaged or toxic proteins, and eliminate damaged organelles via selective autophagy of mitochondria, a process termed mitophagy. Failure of these quality control pathways is implicated in the pathogenesis of Parkinson's disease and other neurodegenerative diseases. Impairment of mitochondrial quality control has been demonstrated to activate innate immune pathways, including inflammasome-mediated signaling and the antiviral cyclic GMP-AMP synthase (cGAS)/stimulator of interferon genes (STING)–regulated interferon response. Immune system malfunction is a common hallmark in many neurodegenerative diseases; however, whether inflammation suppresses or exacerbates disease pathology is still unclear. The goal of this review is to provide a historical overview of the field, describe mechanisms of mitochondrial quality control, and highlight recent advances on the emerging role of mitochondria in innate immunity and inflammation.
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