Mitochondrial biogenesis and fragmentation as regulators of protein degradation in striated muscles.
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".
Dulbecco Telethon Institute at Venetian Institute of Molecular Medicine, via Orus 2, 35129 Padova, Italy. vanina.romanello@unipd.it
Vanina
V
Romanello
Marco
M
Sandri
D000220:Adaptation, Biological; D000818:Animals; D002352:Carrier Proteins / Q000235:genetics / Q000378:metabolism; D004734:Energy Metabolism; D006801:Humans; D008931:Mitochondria, Muscle / Q000235:genetics / Q000378:metabolism*; D018482:Muscle, Skeletal / Q000378:metabolism; D054792:Muscle, Striated / Q000378:metabolism*; D009206:Myocardium / Q000378:metabolism; D059748:Proteolysis
D002352:Carrier Proteins