Cited by 355Muscle Physiology and DisordersMitochondrial Function and PathologyAmyotrophic Lateral Sclerosis Research

Denervation-Induced Skeletal Muscle Atrophy Is Associated with Increased Mitochondrial Ros Production

Muller, Florian L., Song, Wook, Jang, Youngmok C., Liu, Yuhong, Sabia, Marian, Richardson, Arlan, Van Remmen, Holly·2007·American Journal of Physiology-Regulatory, Integrative and Comparative Physiology

Abstract

Reactive oxygen species (ROS), especially mitochondrial ROS, are postulated to play a significant role in muscle atrophy. We report a dramatic increase in mitochondrial ROS generation in three conditions associated with muscle atrophy: in aging, in mice lacking CuZn-SOD (Sod1(-/-)), and in the neurodegenerative disease, amyotrophic lateral sclerosis (ALS). ROS generation in muscle mitochondria is nearly threefold higher in 28- to 32-mo-old than in 10-mo-old mice and is associated with a 30% loss in gastrocnemius mass. In Sod1(-/-) mice, muscle mitochondrial ROS production is increased >100% in 20-mo compared with 5-mo-old mice along with a >50% loss in muscle mass. ALS G93A mutant mice show a 75% loss of muscle mass during disease progression and up to 12-fold higher muscle mitochondrial ROS generation. In a second ALS mutant model, H46RH48Q mice, ROS production is approximately fourfold higher than in control mice and is associated with a less dramatic loss (30%) in muscle mass. Thus ROS production is strongly correlated with the extent of muscle atrophy in these models. Because each of the models of muscle atrophy studied are associated to some degree with a loss of innervation, we were interested in determining whether denervation plays a role in ROS generation in muscle mitochondria isolated from hindlimb muscle following surgical sciatic nerve transection. Seven days post-denervation, muscle mitochondrial ROS production increased nearly 30-fold. We conclude that enhanced generation of mitochondrial ROS may be a common factor in the mechanism underlying denervation-induced atrophy.

Integrity signals

Registry

Crossref · 10.1152/ajpregu.00767.2006

Cites

88 of 88 references verified0 citation errors · 0 not checkable

Statistics

Recomputing p-values needs the paper’s full text.

Claims the paper makes

This paper’s full text isn’t openly available, so its claims and self-check weren’t run. The registry and citation checks still apply.

Claims other papers make about this one

Each is checked against this paper’s own text: does it say what the citing paper says it does?

  • Enhanced generation of mitochondrial ROS may be a common factor in denervation-induced atrophy.

    “Enhanced generation of mitochondrial ROS may be a common factor in the mechanism underlying denervation-induced atrophy [15].”

Cites

Flagged first, then by citations

Cited by

Sorted by citations

Authors
Muller, F. L., Song, W., Jang, Y. C., Liu, Y., Sabia, M., Richardson, A., & Van Remmen, H.
Affiliations
  • Seoul National University (KR)
  • The University of Texas at San Antonio Health Science Center (US)
Venue
American Journal of Physiology-Regulatory, Integrative and Comparative Physiology
Published
2007-09
Volume
293
Issue
3
Pages
R1159-R1168
ISSN
  • 0363-6119 (ISSN-L)
  • 1522-1490
OpenAlex
W2137182040
Cited by
355
References
88
Citations by year
2026: 11 · 2025: 14 · 2024: 16 · 2023: 14 · 2022: 35 · 2021: 23 · 2020: 29 · 2019: 23 · 2018: 25 · 2017: 19 · 2016: 26 · 2015: 18 · 2014: 13 · 2013: 20 · 2012: 16
FWCI
5.03
Type
journal article
Language
en
Open access
closed
Locations
  • American Journal of Physiology-Regulatory, Integrative and Comparative Physiology (publishedVersion)
  • PubMed (publishedVersion)
Funders
National Institute on Aging (5T3 AG 021890 02, P01 AG-20591, P01AG020591, T32AG021890)
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Muscle Physiology and Disorders
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
  • Health Sciences › Medicine › Neurology › Amyotrophic Lateral Sclerosis Research
Keywords
skeletal muscle atrophy, denervation, mitochondrial reactive oxygen species, oxidative stress, sciatic nerve transection, aging, amyotrophic lateral sclerosis, muscle mass loss, hindlimb muscles
MeSH terms
Superoxide Dismutase-1, Amyotrophic Lateral Sclerosis, Animals, Female, Mice, Inbred C57BL, Mitochondria, Muscle, Muscle Denervation, Muscular Atrophy, Organ Size, Oxygen Consumption, Sciatic Nerve, Superoxide Dismutase, Reactive Oxygen Species, Mice, Knockout, Oxidative Stress, Muscle, Skeletal, Mice

About these checks

Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.

Statistics and arithmetic are recomputed, not judged.

Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.

What counts as a claim ›How we measure confidence ›How we check this ›

Are you an author, or do you see a problem with this page? Request a review