title: Receptor-mediated mitophagy.
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.
authors.affiliation: Department of Cardiovascular Medicine, Graduate School of Medicine, Osaka University, Suita, Osaka 565-0871, Japan. Electronic address: yamaguti@cardiology.med.osaka-u.ac.jp.
authors.forename: Osamu
authors.initials: O
authors.lastname: Yamaguchi
authors.affiliation: Department of Cardiovascular Medicine, Graduate School of Medicine, Osaka University, Suita, Osaka 565-0871, Japan.
authors.forename: Tomokazu
authors.initials: T
authors.lastname: Murakawa
authors.affiliation: Cardiovascular Division, King's College London British Heart Foundation Centre of Excellence, London SE5 9NU, United Kingdom.
authors.forename: Kazuhiko
authors.initials: K
authors.lastname: Nishida
authors.affiliation: Cardiovascular Division, King's College London British Heart Foundation Centre of Excellence, London SE5 9NU, United Kingdom.
authors.forename: Kinya
authors.initials: K
authors.lastname: Otsu
mesh_terms: D000818:Animals; D000071183:Autophagy-Related Proteins / Q000378:metabolism; D006801:Humans; D008565:Membrane Proteins / Q000378:metabolism; D008929:Mitochondria, Heart / Q000378:metabolism*; D063306:Mitophagy; D009206:Myocardium / Q000378:metabolism*; D019253:Proto-Oncogene Proteins c-bcl-2 / Q000378:metabolism; D018160:Receptors, Cytoplasmic and Nuclear / Q000378:metabolism*; D044767:Ubiquitin-Protein Ligases / Q000378:metabolism
chemical_list: D000071183:Autophagy-Related Proteins; D008565:Membrane Proteins; D019253:Proto-Oncogene Proteins c-bcl-2; D018160:Receptors, Cytoplasmic and Nuclear; D044767:Ubiquitin-Protein Ligases
keywords: Autophagy; Mitochondrial fusion and fission; Mitophagy; Receptor