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

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.

Automated summary

Mitophagy is an essential cellular process that regulates mitochondrial quantity through autophagy, with BNIP3L/Nix serving as a receptor. BNIP3L is involved in various physiological and pathological processes and is crucial in the induction of mitophagy. This review provides an overview of BNIP3L-mediated mitophagy, its molecular regulation, and its potential role in human diseases such as cancer and neurological disorders.