Receptor-mediated mitophagy. (June 2016)

• Record Type: Journal Article
• Authors: Yamaguchi, Osamu; Murakawa, Tomokazu; Nishida, Kazuhiko; Otsu, Kinya
• Is Part Of: Journal of molecular and cellular cardiology. Volume 95(2016:Jun.)
• Page Start: 50
• Page End: 56
• Publication Date: 2016-06
• Subjects: AAA ATPases associated with diverse cellular activities -- ADP adenosine diphosphate -- ANT adenine nucleotide translocator -- Atg autophagy related -- ATP adenosine triphosphate -- BNIP3 adenovirus E1B-19 kDa-interacting protein 3 -- BNIP3L adenovirus E1B-19 kDa-interacting protein 3 like -- CCCP carbonyl cyanide m-chlorophenyl hydrazine -- CUET coupling of ubiquitin endoplasmic reticulum degradation domain targeting -- DNA deoxyribonucleic acid -- Drp1 dynamin-related protein 1 -- LC3 homolog of microtubule-associated protein 1 light chain 3 -- LIR LC3-interacting region -- MDVs mitochondria-derived vesicles -- Mfn mitofusin -- NIX NIP3-like protein X -- OPA1 Optic atrophy 1 -- PINK1 phosphatase and tensin homolog-induced putative protein kinase 1 -- ROS reactive oxygen species -- SMURF1 Smad-ubiquitin regulatory factor 1 -- VDAC1 voltage-dependent anion channel 1; Autophagy -- Mitophagy -- Mitochondrial fusion and fission -- Receptor; Cardiology -- Periodicals; Heart Diseases -- Periodicals; Molecular Biology -- Periodicals; Cardiologie -- Périodiques; Cardiology; Electronic journals; Periodicals; 616.12
• DOI: 10.1016/j.yjmcc.2016.03.010
• Languages: English
• ISSNs: 0022-2828

Abstract

Abstract: Mitochondria are essential organelles that supply ATP through oxidative phosphorylation to maintain cellular homeostasis. Extrinsic or intrinsic agents can impair mitochondria, and these impaired mitochondria can generate reactive oxygen species (ROS) as byproducts, inducing cellular damage and cell death. The quality control of mitochondria is essential for the maintenance of normal cellular functions, particularly in cardiomyocytes, because they are terminally differentiated. Accumulation of damaged mitochondria is characteristic of various diseases, including heart failure, neurodegenerative disease, and aging-related diseases. Mitochondria are generally degraded through autophagy, an intracellular degradation system that is conserved from yeast to mammals. Autophagy is thought to be a nonselective degradation process in which cytoplasmic proteins and organelles are engulfed by isolation membrane to form autophagosomes in eukaryotic cells. However, recent studies have described the process of selective autophagy, which targets specific proteins or organelles such as mitochondria. Mitochondria-specific autophagy is called mitophagy. Dysregulation of mitophagy is implicated in the development of chronic diseases including neurodegenerative diseases, metabolic diseases, and heart failure. In this review, we discuss recent progress in research on mitophagy receptors. Highlights: Mitochondrial elimination is mediated through mitophagy. Mitophagy is important for maintaining cellular and organ homeostasis. Receptors on the outer mitochondrial membrane play an important role in mitophagy. BCL2L13 has roles both in mitochondrial fission and as a mitophagy receptor.