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Mitochondrial Biogenesis and Fragmentation as Regulators of Muscle Protein Degradation

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Abstract

Mitochondria form a dynamic network that rapidly adapts to cellular energy demand. This adaptation is particularly important in skeletal muscle because of its high metabolic rate. Indeed, muscle energy level is one of the cellular checkpoints that lead either to sustained protein synthesis and growth or protein breakdown and atrophy. Mitochondrial function is affected by changes in shape, number, and localization. The dynamics that control the mitochondrial network, such as biogenesis and fusion, or fragmentation and fission, ultimately affect the signaling pathways that regulate muscle mass. Regular exercise and healthy muscles are important players in the metabolic control of human body. Indeed, a sedentary lifestyle is detrimental for muscle function and is one of the major causes of metabolic disorders such as obesity and diabetes. This article reviews the rapid progress made in the past few years regarding the role of mitochondria in the control of proteolytic systems and in the loss of muscle mass and function.

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Acknowledgments

We apologize to colleagues whose studies were not cited owing to space limitations. Our work is supported by grants from ASI (OSMA project), Telethon-Italy (TCP04009), from the European Union (MYOAGE, contract: 223576 of FP7), AFM (14135), and the Italian Ministry of Education, University and Research (PRIN 2007). The critical reading of Kenneth Dyar is gratefully acknowledged.

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No potential conflicts of interest relevant to this article were reported.

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Authors and Affiliations

  1. Venetian Institute of Molecular Medicine, Via Orus 2, 35129, Padova, Italy

    Marco Sandri

  2. Dulbecco Telethon Institute at Venetian Institute of Molecular Medicine, via Orus 2, 35129, Padova, Italy

    Vanina Romanello

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  1. Vanina Romanello
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  2. Marco Sandri
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Correspondence to Marco Sandri.

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Romanello, V., Sandri, M. Mitochondrial Biogenesis and Fragmentation as Regulators of Muscle Protein Degradation. Curr Hypertens Rep 12, 433–439 (2010). https://doi.org/10.1007/s11906-010-0157-8

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