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

• Published in: Cell death & disease Vol. 13; no. 1; pp. 14 - 11
• Main Authors: Li, Yue, Zheng, Wanqing, Lu, Yangyang, Zheng, Yanrong, Pan, Ling, Wu, Xiaoli, Yuan, Yang, Shen, Zhe, Ma, Shijia, Zhang, Xingxian, Wu, Jiaying, Chen, Zhong, Zhang, Xiangnan
• Format: Journal Article
• Language: English
• Published: London Nature Publishing Group UK 20-12-2021; Springer Nature B.V; Nature Publishing Group
• Subjects: 13; 14; 14/34; 631/67; 631/80/39/2348; 82; Amyotrophic Lateral Sclerosis - metabolism; Animals; Antibodies; Apoptosis; Autophagosomes - metabolism; Autophagy; Biochemistry; Biomedical and Life Sciences; Biosynthesis; Brain Injuries, Traumatic - metabolism; Cancer; Cell Biology; Cell Culture; Cerebral Hemorrhage - metabolism; Disease; Homeostasis; Humans; Hypoxia; Immunology; Laboratories; Life Sciences; Membrane proteins; Membrane Proteins - metabolism; Metabolism; Mitochondria; Mitochondria - metabolism; Mitochondrial Membranes - metabolism; Mitochondrial Proteins - metabolism; Mitophagy; Molecular modelling; Neoplasms - metabolism; Neurological diseases; Neurological disorders; Neurosciences; Parkinson Disease - metabolism; Permeability; Phagocytosis; Phagosomes; Proteins; Proto-Oncogene Proteins - metabolism; Quality control; Reticulocytes; Review; Review Article; Signal Transduction; Tumor Suppressor Proteins - metabolism
• ISSN: 2041-4889; 2041-4889
• DOI: 10.1038/s41419-021-04469-y

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.