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Oxidative Medicine and Cellular Longevity
Volume 2017, Article ID 3292087, 13 pages
Review Article

Disrupted Skeletal Muscle Mitochondrial Dynamics, Mitophagy, and Biogenesis during Cancer Cachexia: A Role for Inflammation

Integrative Muscle Biology Laboratory, Department of Exercise Science, University of South Carolina, Columbia, SC, USA

Correspondence should be addressed to James A. Carson; ude.cs.xobliam@jnosrac

Received 31 March 2017; Revised 6 June 2017; Accepted 19 June 2017; Published 13 July 2017

Academic Editor: Moh H. Malek

Copyright © 2017 Brandon N. VanderVeen et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Chronic inflammation is a hallmark of cancer cachexia in both patients and preclinical models. Cachexia is prevalent in roughly 80% of cancer patients and accounts for up to 20% of all cancer-related deaths. Proinflammatory cytokines IL-6, TNF-α, and TGF-β have been widely examined for their regulation of cancer cachexia. An established characteristic of cachectic skeletal muscle is a disrupted capacity for oxidative metabolism, which is thought to contribute to cancer patient fatigue, diminished metabolic function, and muscle mass loss. This review’s primary objective is to highlight emerging evidence linking cancer-induced inflammation to the dysfunctional regulation of mitochondrial dynamics, mitophagy, and biogenesis in cachectic muscle. The potential for either muscle inactivity or exercise to alter mitochondrial dysfunction during cancer cachexia will also be discussed.