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Biological Chemistry

Editor-in-Chief: Brüne, Bernhard

Editorial Board Member: Buchner, Johannes / Lei, Ming / Ludwig, Stephan / Sies, Helmut / Thomas, Douglas D. / Turk, Boris / Wittinghofer, Alfred

12 Issues per year


IMPACT FACTOR 2016: 3.273

CiteScore 2016: 3.01

SCImago Journal Rank (SJR) 2016: 1.679
Source Normalized Impact per Paper (SNIP) 2016: 0.800

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1437-4315
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Volume 394, Issue 3 (Mar 2013)

Issues

Mitochondrial pathways in sarcopenia of aging and disuse muscle atrophy

Riccardo Calvani / Anna-Maria Joseph
  • Department of Aging and Geriatric Research, Institute on Aging, University of Florida, Gainesville, FL 32610, USA
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/ Peter J. Adhihetty
  • Department of Applied Physiology and Kinesiology, University of Florida, Gainesville, FL 32611, USA
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/ Alfredo Miccheli / Maurizio Bossola
  • Department of Surgery, Catholic University of the Sacred Heart School of Medicine, Rome 00168, Italy
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/ Christiaan Leeuwenburgh
  • Department of Aging and Geriatric Research, Institute on Aging, University of Florida, Gainesville, FL 32610, USA
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/ Roberto Bernabei
  • Department of Geriatrics, Neurosciences and Orthopedics, Catholic University of the Sacred Heart School of Medicine, Rome 00168, Italy
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/ Emanuele Marzetti
  • Corresponding author
  • Department of Geriatrics, Neurosciences and Orthopedics, Catholic University of the Sacred Heart School of Medicine, Rome 00168, Italy
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Published Online: 2013-02-02 | DOI: https://doi.org/10.1515/hsz-2012-0247

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

About the article

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


Received: 2012-07-06

Accepted: 2012-11-13

Published Online: 2013-02-02

Published in Print: 2013-03-01


Citation Information: Biological Chemistry, ISSN (Online) 1437-4315, ISSN (Print) 1431-6730, DOI: https://doi.org/10.1515/hsz-2012-0247.

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©2013 by Walter de Gruyter Berlin Boston. Copyright Clearance Center

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