Mitochondrial autophagy: Origins, significance, and role of BNIP3 and NIX

Biochim Biophys Acta. 2015 Oct;1853(10 Pt B):2775-83. doi: 10.1016/j.bbamcr.2015.02.022. Epub 2015 Mar 6.

Abstract

Mitochondrial autophagy (mitophagy) is a core cellular activity. In this review, we consider mitophagy and related cellular processes and discuss their significance for human disease. Strong parallels exist between mitophagy and xenophagy employed in host defense. These mechanisms converge on receptors in the innate immune system in clinically relevant scenarios. Mitophagy is part of a cellular quality control mechanism, which is implicated in degenerative disease, especially neurodegenerative disease. Furthermore, mitophagy is an aspect of cellular remodeling, which is employed during development. BNIP3 and NIX are related multi-functional outer mitochondrial membrane proteins. BNIP3 regulates mitophagy during hypoxia, whereas NIX is required for mitophagy during development of the erythroid lineage. Recent advances in the field of BNIP3- and NIX-mediated mitophagy are discussed.

Keywords: Autophagy; BNIP3; Erythrocyte; Mitochondrion; NIX; Necrosis.

Publication types

  • Research Support, N.I.H., Extramural
  • Review

MeSH terms

  • Animals
  • Autophagy / physiology*
  • Cell Hypoxia / physiology
  • Erythroid Cells / cytology
  • Erythroid Cells / metabolism*
  • Humans
  • Membrane Proteins / genetics
  • Membrane Proteins / metabolism*
  • Mitochondria / genetics
  • Mitochondria / metabolism*
  • Mitochondrial Membranes / metabolism
  • Mitophagy / physiology*
  • Proto-Oncogene Proteins / genetics
  • Proto-Oncogene Proteins / metabolism*
  • Tumor Suppressor Proteins / genetics
  • Tumor Suppressor Proteins / metabolism*

Substances

  • BNIP3 protein, human
  • BNIP3L protein, human
  • Membrane Proteins
  • Proto-Oncogene Proteins
  • Tumor Suppressor Proteins