Mitochondrial biogenesis and fragmentation as regulators of protein degradation in striated muscles |
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| Institution: | 1. Department of Biology, University of Copenhagen, Denmark;2. Core Facility for Integrated Microscopy, Department of Biomedical Sciences, University of Copenhagen, Denmark;1. Department of Chemical and Systems Biology, Stanford University School of Medicine, Stanford, CA, United States;2. Department of Cardiology and Pneumology, Gottingen University Medical Center, Gottingen, Germany;3. DZHK (German Center for Cardiovascular Research), partner site Gottingen, Germany;4. Department of Pediatrics division of Critical Care Medicine, Stanford University School of Medicine, Stanford, CA, United States |
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| Abstract: | Mitochondria are dynamic organelles which adapt their morphology by fusion and fission events to the bioenergetic requirements of the cell. Cardiac and skeletal muscles are tissues with high energy demand and mitochondrial plasticity plays a key role in the homeostasis of these cells. Indeed, alterations in mitochondrial morphology, distribution and function are common features in catabolic conditions. Moreover, dysregulation of mitochondrial dynamics affects the signaling pathways that regulate muscle mass. This review discusses the recent findings of the role of mitochondrial fusion/fission and mitophagy in the control of proteolytic pathways. This article is part of a special issue entitled "Focus on Cardiac Metabolism". |
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