title: Mitochondrial autophagy: Origins, significance, and role of BNIP3 and NIX.
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.
authors.affiliation: Department of Cell & Molecular Biology, Lindsley F. Kimball Research Institute, New York Blood Center, 310 East 67 Street, New York, NY 10065-6275, USA. Electronic address: pney@nybloodcenter.org.
authors.forename: Paul A
authors.initials: PA
authors.lastname: Ney
mesh_terms: D000818:Animals; D001343:Autophagy / Q000502:physiology*; D015687:Cell Hypoxia / Q000502:physiology; D041905:Erythroid Cells / Q000166:cytology / Q000378:metabolism*; D006801:Humans; D008565:Membrane Proteins / Q000235:genetics / Q000378:metabolism*; D008928:Mitochondria / Q000235:genetics / Q000378:metabolism*; D051336:Mitochondrial Membranes / Q000378:metabolism; D063306:Mitophagy / Q000502:physiology*; D011518:Proto-Oncogene Proteins / Q000235:genetics / Q000378:metabolism*; D025521:Tumor Suppressor Proteins / Q000235:genetics / Q000378:metabolism*
chemical_list: C090121:BNIP3 protein, human; C116838:BNIP3L protein, human; D008565:Membrane Proteins; D011518:Proto-Oncogene Proteins; D025521:Tumor Suppressor Proteins
keywords: Autophagy; BNIP3; Erythrocyte; Mitochondrion; NIX; Necrosis