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

Yue Li, Wanqing Zheng, Yangyang Lu, Yanrong Zheng, Ling Pan, Xiaoli Wu, Yang Yuan, Zhe Shen, Shijia Ma, Xingxian Zhang, Jiaying Wu, Zhong Chen, Xiangnan Zhang

2021Cell Death and Disease191 citationsDOIOpen Access PDF

Abstract

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.

Topics & Concepts

MitophagyAutophagyMitochondrionCell biologyBiologyNeuroscienceChemistryBiochemistryApoptosisAutophagy in Disease and TherapyUbiquitin and proteasome pathwaysMitochondrial Function and Pathology
BNIP3L/NIX-mediated mitophagy: molecular mechanisms and implications for human disease | Litcius