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Biological Chemistry

Editor-in-Chief: Brüne, Bernhard

Editorial Board Member: Buchner, Johannes / Ludwig, Stephan / Sies, Helmut / Turk, Boris / Wittinghofer, Alfred

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Mitochondrial pathways in sarcopenia of aging and disuse muscle atrophy

Riccardo Calvani1 / Anna-Maria Joseph2 / Peter J. Adhihetty3 / Alfredo Miccheli4 / Maurizio Bossola5 / Christiaan Leeuwenburgh2 / Roberto Bernabei6 / 6

1Institute of Crystallography, Italian National Research Council (CNR), Bari 70126, Italy

2Department of Aging and Geriatric Research, Institute on Aging, University of Florida, Gainesville, FL 32610, USA

3Department of Applied Physiology and Kinesiology, University of Florida, Gainesville, FL 32611, USA

4Department of Chemistry, “Sapienza” University of Rome, Rome 00185, Italy

5Department of Surgery, Catholic University of the Sacred Heart School of Medicine, Rome 00168, Italy

6Department of Geriatrics, Neurosciences and Orthopedics, Catholic University of the Sacred Heart School of Medicine, Rome 00168, Italy

Corresponding author: Emanuele Marzetti, Department of Geriatrics, Neurosciences and Orthopedics, Catholic University of the Sacred Heart School of Medicine, Rome 00168, Italy

Citation Information: Biological Chemistry. Volume 394, Issue 3, Pages 393–414, ISSN (Online) 1437-4315, ISSN (Print) 1431-6730, DOI: 10.1515/hsz-2012-0247, February 2013

Publication History

Received:
2012-07-06
Accepted:
2012-11-13
Published Online:
2013-02-02

Abstract

Muscle loss during aging and disuse is a highly prevalent and disabling condition, but knowledge about cellular pathways mediating muscle atrophy is still limited. Given the postmitotic nature of skeletal myocytes, the maintenance of cellular homeostasis relies on the efficiency of cellular quality control mechanisms. In this scenario, alterations in mitochondrial function are considered a major factor underlying sarcopenia and muscle atrophy. Damaged mitochondria are not only less bioenergetically efficient, but also generate increased amounts of reactive oxygen species, interfere with cellular quality control mechanisms, and display a greater propensity to trigger apoptosis. Thus, mitochondria stand at the crossroad of signaling pathways that regulate skeletal myocyte function and viability. Studies on these pathways have sometimes provided unexpected and counterintuitive results, which suggests that they are organized into a complex, heterarchical network that is currently insufficiently understood. Untangling the complexity of such a network will likely provide clinicians with novel and highly effective therapeutics to counter the muscle loss associated with aging and disuse. In this review, we summarize the current knowledge on the mechanisms whereby mitochondrial dysfunction intervenes in the pathogenesis of sarcopenia and disuse atrophy, and highlight the prospect of targeting specific processes to treat these conditions.

Keywords: apoptosis; autophagy; fission; fusion; mitophagy; oxidative stress

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