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Neutralizing mitochondrial ROS does not rescue muscle atrophy induced by hindlimb unloading in female mice.

Authors
  • Eshima, Hiroaki1, 2
  • Siripoksup, Piyarat1, 2
  • Mahmassani, Ziad S1, 2
  • Johnson, Jordan M1, 3
  • Ferrara, Patrick J1, 3
  • Verkerke, Anthony R P1, 3
  • Salcedo, Anahy2
  • Drummond, Micah J1, 4
  • Funai, Katsuhiko1, 4
  • 1 Department of Physical Therapy and Athletic Training, University of Utah, Salt Lake City, Utah.
  • 2 Diabetes and Metabolism Research Center, University of Utah, Salt Lake City, Utah.
  • 3 Department of Nutrition and Integrative Physiology, University of Utah, Salt Lake City, Utah.
  • 4 Molecular Medicine Program, University of Utah, Salt Lake City, Utah.
Type
Published Article
Journal
Journal of Applied Physiology
Publisher
American Physiological Society
Publication Date
Jul 01, 2020
Volume
129
Issue
1
Pages
124–132
Identifiers
DOI: 10.1152/japplphysiol.00456.2019
PMID: 32552434
Source
Medline
Keywords
Language
English
License
Unknown

Abstract

Excess reactive oxygen species (ROS) induced by physical inactivity is associated with muscle atrophy and muscle weakness. However, the role of mitochondrial ROS on disuse-induced muscle atrophy is not fully understood. The purpose of this study was to utilize a genetic strategy to examine the effect of neutralizing mitochondrial ROS on disuse-induced skeletal muscle atrophy. This was accomplished by placing wild-type (WT) and mitochondrial-targeted catalase-expressing (MCAT) littermate mice on 7 days of hindlimb unloading. After assessment of body weight and composition, muscles were analyzed for individual muscle mass, force-generating capacity, fiber type, cross-sectional area, and mitochondrial function, including H2O2 production. Despite a successful attenuation of mitochondrial ROS, MCAT mice were not protected from muscle atrophy. No differences were observed in body composition, lean mass, individual muscle masses, force-generating capacity, or muscle fiber cross-sectional area. These data suggest that neutralizing mitochondrial ROS is insufficient to suppress disuse-induced loss of skeletal muscle mass and contractile function.NEW & NOTEWORTHY The premise of this study was to examine the efficacy of genetic suppression of mitochondrial reactive oxygen species (ROS) to attenuate disuse-induced muscle atrophy and muscle weakness. Neutralization of mitochondrial ROS by MCAT expression was insufficient to rescue muscle atrophy and muscle weakness.

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