BNIP3L/NIX-mediated mitophagy: molecular mechanisms and implications for human disease

被引:104
作者
Li, Yue [1 ]
Zheng, Wanqing [1 ]
Lu, Yangyang [1 ]
Zheng, Yanrong [1 ,2 ]
Pan, Ling [1 ]
Wu, Xiaoli [1 ]
Yuan, Yang [1 ]
Shen, Zhe [1 ]
Ma, Shijia [1 ]
Zhang, Xingxian [1 ]
Wu, Jiaying [3 ]
Chen, Zhong [1 ,2 ]
Zhang, Xiangnan [1 ]
机构
[1] Zhejiang Univ, Inst Pharmacol & Toxicol, Coll Pharmaceut Sci, Key Lab Med Neurobiol,Minist Hlth China, Hangzhou, Peoples R China
[2] Zhejiang Chinese Med Univ, Coll Pharmacol Sci, Key Lab Neuropharmacol & Translat Med Zhejiang Pr, Hangzhou, Peoples R China
[3] Zhejiang Univ, Affiliated Hosp 1, Dept Pharm, Sch Med, Hangzhou, Peoples R China
基金
中国国家自然科学基金;
关键词
HYPOXIA-INDUCED AUTOPHAGY; BREAST-CANCER CELLS; UP-REGULATION; MITOCHONDRIAL CLEARANCE; CALCIUM HOMEOSTASIS; MEDIATED MITOPHAGY; BH3-ONLY PROTEINS; NEURONAL DEATH; IN-VIVO; NIX;
D O I
10.1038/s41419-021-04469-y
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
Mitophagy is a highly conserved cellular process that maintains the mitochondrial quantity by eliminating dysfunctional or superfluous mitochondria through autophagy machinery. The mitochondrial outer membrane protein BNIP3L/Nix serves as a mitophagy receptor by recognizing autophagosomes. BNIP3L is initially known to clear the mitochondria during the development of reticulocytes. Recent studies indicated it also engages in a variety of physiological and pathological processes. In this review, we provide an overview of how BNIP3L induces mitophagy and discuss the biological functions of BNIP3L and its regulation at the molecular level. We further discuss current evidence indicating the involvement of BNIP3L-mediated mitophagy in human disease, particularly in cancer and neurological disorders.
引用
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页数:11
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