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Mitochondrial fission and remodelling contributes to muscle atrophy

Romanello, Vanina
Guadagnin, Eleonora
Gomes, Ligia
Roder, Ira
Sandri, Claudia
Petersen, Yvonne
Milan, Giulia
Masiero, Eva
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Published in EMBO Journal. 2010, vol. 29, no. 10, p. 1774-1785
Abstract Mitochondria are crucial organelles in the production of energy and in the control of signalling cascades. A machinery of pro-fusion and fission proteins regulates their morphology and subcellular localization. In muscle this results in an orderly pattern of intermyofibrillar and subsarcolemmal mitochondria. Muscular atrophy is a genetically controlled process involving the activation of the autophagy-lysosome and the ubiquitin-proteasome systems. Whether and how the mitochondria are involved in muscular atrophy is unknown. Here, we show that the mitochondria are removed through autophagy system and that changes in mitochondrial network occur in atrophying muscles. Expression of the fission machinery is per se sufficient to cause muscle wasting in adult animals, by triggering organelle dysfunction and AMPK activation. Conversely, inhibition of the mitochondrial fission inhibits muscle loss during fasting and after FoxO3 overexpression. Mitochondrial-dependent muscle atrophy requires AMPK activation as inhibition of AMPK restores muscle size in myofibres with altered mitochondria. Thus, disruption of the mitochondrial network is an essential amplificatory loop of the muscular atrophy programme.
Keywords AMP-Activated Protein Kinases/metabolismAnimalsAutophagyCell LineHumansMiceMicroscopy, Fluorescence/methodsMitochondria/*metabolismModels, BiologicalMuscle, Skeletal/pathologyMuscular Atrophy/*pathologyRNA InterferenceSignal TransductionTime FactorsTransfection
PMID: 20400940
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Research group Les mitochondries dans la vie cellulaire (850)
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ROMANELLO, Vanina et al. Mitochondrial fission and remodelling contributes to muscle atrophy. In: EMBO Journal, 2010, vol. 29, n° 10, p. 1774-1785. doi: 10.1038/emboj.2010.60 https://archive-ouverte.unige.ch/unige:21264

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Deposited on : 2012-05-23

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