Evidence map›Paper›PMID 23729587›Full record

ArticleFASEB journal : official publication of the Federation of American Societies for Experimental Biology2013

CuZnSOD gene deletion targeted to skeletal muscle leads to loss of contractile force but does not cause muscle atrophy in adult mice.

Yiqiang Zhang, Carol Davis, George K Sakellariou, Yun Shi, Anna C Kayani, Daniel Pulliam, Arunabh Bhattacharya, Arlan Richardson, Malcolm J Jackson, Anne McArdle and 2 more

Open access · greenAbstract read
In one paragraph

Article in FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers.

0numbers the graph read from it
0cells of the map it votes in
53citing papers in PubMed
3.1field-weighted citation impact, top 8% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

53 citing papers in PubMed, 76 citations in OpenAlex.

  1. Molecular Framework of the Onset and Progression of Skeletal Muscle Aging.International journal of molecular sciences · 2025
    Review
  2. Review
  3. Reactive oxygen species in the pathogenesis of sarcopenia.Free radical biology & medicine · 2025
    Review
  4. Effects of aging on calcium channels in skeletal muscle.Frontiers in molecular biosciences · 2025
    Review
  5. Article
  6. Review
  7. Article
  8. Article
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  10. Article
  11. Article
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  15. Article
  16. Redox Signaling and Sarcopenia: Searching for the Primary Suspect.International journal of molecular sciences · 2021
    Review
  17. Review
  18. Article
  19. Article
  20. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

12 authors at 4 institutions in 2 countries.

Yiqiang ZhangDepartment of Physiology, University of Texas Health Science Center, San Antonio, Texas 78249, USA.
Carol Davis
George K Sakellariou
Yun Shi
Anna C Kayani
Daniel Pulliam
Arunabh Bhattacharya
Arlan Richardson
Malcolm J Jackson
Anne McArdle
Susan V Brooks
Holly Van Remmen
The University of Texas Health Science Center at San Antonio · USUniversity of Liverpool · GBLongevity Biotech (United States) · USUniversity of Michigan–Ann Arbor · US

Funding

Research DevelopmentP30AG013283 · NIA · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI MILLER, RICHARD A · 1995 to 2014
$12.3M
TRANSGENIC ANIMAL CORE SUBCONTRACT WITH UTHSC AT SAN ANTONIOP01AG020591 · NIA · UNIVERSITY OF TEXAS HLTH SCI CTR SAN ANT · PI BROOKS, SUSAN V · 2002 to 2014
$10.7M
BLRD VA I01 BX000517Medical Research Council G0700919Medical Research Council MR/K006312/1NIA NIH HHS AG-020591NIA NIH HHS P01 AG020591NIA NIH HHS P30 AG013283
6 · The paper itself

Abstract

We have previously shown that deletion of CuZnSOD in mice (Sod1(-/-) mice) leads to accelerated loss of muscle mass and contractile force during aging. To dissect the relative roles of skeletal muscle and motor neurons in this process, we used a Cre-Lox targeted approach to establish a skeletal muscle-specific Sod1-knockout (mKO) mouse to determine whether muscle-specific CuZnSOD deletion is sufficient to cause muscle atrophy. Surprisingly, mKO mice maintain muscle masses at or above those of wild-type control mice up to 18 mo of age. In contrast, maximum isometric specific force measured in gastrocnemius muscle is significantly reduced in the mKO mice. We found no detectable increases in global measures of oxidative stress or ROS production, no reduction in mitochondrial ATP production, and no induction of adaptive stress responses in muscle from mKO mice. However, Akt-mTOR signaling is elevated and the number of muscle fibers with centrally located nuclei is increased in skeletal muscle from mKO mice, which suggests elevated regenerative pathways. Our data demonstrate that lack of CuZnSOD restricted to skeletal muscle does not lead to muscle atrophy but does cause muscle weakness in adult mice and suggest loss of CuZnSOD may potentiate muscle regenerative pathways.

Indexed as

AnimalsBlotting, WesternLipid PeroxidationMiceMice, KnockoutMicroscopy, Electron, TransmissionMicroscopy, FluorescenceMuscle ContractionMuscle, SkeletalMuscular AtrophyOxidative StressSuperoxide DismutaseSuperoxide Dismutase-1Tyrosine3-nitrotyrosineSod1 protein, mouseSuperoxide DismutaseSuperoxide Dismutase-1Tyrosinecentral nucleioxidative stressregeneration

Identifiers

PMID23729587
PMCPMC3752542
OpenAlexW2156315357

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.