Molecular mechanisms and physiological functions of mitophagy |
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Authors: | Mashun Onishi Koji Yamano Miyuki Sato Noriyuki Matsuda Koji Okamoto |
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Affiliation: | 1. Laboratory of Mitochondrial Dynamics, Graduate School of Frontier Biosciences, Osaka University, Suita Japan ; 2. The Ubiquitin Project, Tokyo Metropolitan Institute of Medical Science, Tokyo Japan ; 3. Laboratory of Molecular Membrane Biology, Institute for Molecular and Cellular Regulation, Gunma University, Maebashi Japan |
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Abstract: | Degradation of mitochondria via a selective form of autophagy, named mitophagy, is a fundamental mechanism conserved from yeast to humans that regulates mitochondrial quality and quantity control. Mitophagy is promoted via specific mitochondrial outer membrane receptors, or ubiquitin molecules conjugated to proteins on the mitochondrial surface leading to the formation of autophagosomes surrounding mitochondria. Mitophagy‐mediated elimination of mitochondria plays an important role in many processes including early embryonic development, cell differentiation, inflammation, and apoptosis. Recent advances in analyzing mitophagy in vivo also reveal high rates of steady‐state mitochondrial turnover in diverse cell types, highlighting the intracellular housekeeping role of mitophagy. Defects in mitophagy are associated with various pathological conditions such as neurodegeneration, heart failure, cancer, and aging, further underscoring the biological relevance. Here, we review our current molecular understanding of mitophagy, and its physiological implications, and discuss how multiple mitophagy pathways coordinately modulate mitochondrial fitness and populations. |
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Keywords: | autophagy mitochondria phosphorylation quality and quantity control ubiquitin |
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