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

Journal

BIOCHIMICA ET BIOPHYSICA ACTA-MOLECULAR CELL RESEARCH
Volume 1853, Issue 10, Pages 2775-2783

Publisher

ELSEVIER SCIENCE BV
DOI: 10.1016/j.bbamcr.2015.02.022

Keywords

BNIP3; NIX; Mitochondrion; Autophagy; Necrosis; Erythrocyte

Funding

  1. National Institutes of Health [R21 DK074519]
  2. American Society of Hematology Bridge Grant
  3. F.M. Kirby Foundation
  4. New York Blood Center

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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 etythroid lineage. Recent advances in the field of BNIP3- and NIX-mediated mitophagy are discussed. This article is part of a Special Issue entitled: Mitophagy. (C) 2015 Elsevier B.V. All rights reserved.

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