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作者机构:German Canc Res Ctr Lysosomal Syst Biol Heidelberg Germany German Canc Res Ctr Syst Biol Cell Death Mech Heidelberg Germany Univ Heidelberg Hosp Dept Surg Heidelberg Germany Heidelberg Univ Bioquant INF 267BQ0045 D-69120 Heidelberg Germany
出 版 物:《CELLULAR AND MOLECULAR LIFE SCIENCES》 (细胞和分子生命科学)
年 卷 期:2016年第73卷第4期
页 面:775-795页
核心收录:
学科分类:0710[理学-生物学] 07[理学] 09[农学]
基 金:German Cancer Research Center (DKFZ), through SBCancer within the Helmholtz Alliance on Systems Biology - Initiative and Networking Fund of the Helmholtz Association (NRB) ImmunoQuant Grant [0316170B] Federal Ministry of Education and Research, Germany [0316191 'LysoSys']
主 题:Bnip3 FUNDC1 LC3-interacting region (LIR) Macroautophagy Mitophagy Nix Parkin E3 ligase Ubiquitin
摘 要:Mitochondria are an essential source of ATP for cellular function, but when damaged, mitochondria generate a plethora of stress signals, which lead to cellular dysfunction and eventually programmed cell death. Thus, a major component of maintaining cellular homeostasis is the recognition and removal of dysfunctional mitochondria through autophagy-mediated degradation, i.e., mitophagy. Mitophagy further constitutes a developmental program, and undergoes a high degree of crosstalk with apoptosis. Reduced mitochondrial quality control is linked to disease pathogenesis, suggesting the importance of process elucidation as a clinical target. Recent work has revealed multiple mitophagy programs that operate independently or undergo crosstalk, and require modulated autophagy receptor activities at outer membranes of mitochondria. Here, we review these mitophagy programs, focusing on pathway mechanisms which recognize and target mitochondria for sequestration by autophagosomes, as well as mechanisms controlling pathway activities. Furthermore, we provide an introduction to the currently available methods for detecting mitophagy.