Evidence map›Paper›PMID 20040516›Full record

ArticleFASEB journal : official publication of the Federation of American Societies for Experimental Biology2010

Increased superoxide in vivo accelerates age-associated muscle atrophy through mitochondrial dysfunction and neuromuscular junction degeneration.

Youngmok C Jang, Michael S Lustgarten, Yuhong Liu, Florian L Muller, Arunabh Bhattacharya, Hanyu Liang, Adam B Salmon, Susan V Brooks, Lisa Larkin, Christopher R Hayworth 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, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 199 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
199citing papers in PubMed, 1 pooled it
6.3field-weighted citation impact, top 3% 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

199 citing papers in PubMed, 1 synthesis or guideline pooled it, 291 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Article
  4. Article
  5. Article
  6. Review
  7. Article
  8. Review
  9. How to measure and model cardiovascular aging.Cardiovascular research · 2025
    Review
  10. Review
  11. Review
  12. Qigu capsule alleviates dexamethasone-induced muscle dysfunction through mitochondrial biogenesis.Journal of traditional Chinese medicine = Chung i tsa chih ying wen pan · 2025
    Article
  13. Article
  14. Review
  15. Reactive oxygen species in the pathogenesis of sarcopenia.Free radical biology & medicine · 2025
    Review
  16. Article
  17. Article
  18. Article
  19. Review
  20. Article

139 more citing papers are in PubMed but not listed here.

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 3 countries.

Youngmok C JangDepartment of Cellular and Structural Biology, University of Texas Health Science Center at San Antonio, San Antonio, TX 78245, USA.
Michael S Lustgarten
Yuhong Liu
Florian L Muller
Arunabh Bhattacharya
Hanyu Liang
Adam B Salmon
Susan V Brooks
Lisa Larkin
Christopher R Hayworth
Arlan Richardson
Holly Van Remmen
South Texas Veterans Health Care System · USUniversity of Michigan–Ann Arbor · USCzech Academy of Sciences, Institute of Physiology · CZThe University of Texas at Austin · US

Funding

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
NIA NIH HHS P01 AG020591NIA NIH HHS P01AG020591
6 · The paper itself

Abstract

Oxidative stress has been implicated in the etiology of age-related muscle loss (sarcopenia). However, the underlying mechanisms by which oxidative stress contributes to sarcopenia have not been thoroughly investigated. To directly examine the role of chronic oxidative stress in vivo, we used a mouse model that lacks the antioxidant enzyme CuZnSOD (Sod1). Sod1(-/-) mice are characterized by high levels of oxidative damage and an acceleration of sarcopenia. In the present study, we demonstrate that muscle atrophy in Sod1(-/-) mice is accompanied by a progressive decline in mitochondrial bioenergetic function and an elevation of mitochondrial generation of reactive oxygen species. In addition, Sod1(-/-) muscle exhibits a more rapid induction of mitochondrial-mediated apoptosis and loss of myonuclei. Furthermore, aged Sod1(-/-) mice show a striking increase in muscle mitochondrial content near the neuromuscular junctions (NMJs). Despite the increase in content, the function of mitochondria is significantly impaired, with increased denervated NMJs and fragmentation of acetylcholine receptors. As a consequence, contractile force in aged Sod1(-/-) muscles is greatly diminished. Collectively, we show that Sod1(-/-) mice display characteristics of normal aging muscle in an accelerated manner and propose that the superoxide-induced NMJ degeneration and mitochondrial dysfunction are potential mechanisms of sarcopenia.

Indexed as

Age FactorsAgingAnimalsApoptosisCaspase 3Cell NucleusMiceMice, Mutant StrainsMitochondria, MuscleMuscle ContractionMuscle Fibers, SkeletalNeuromuscular JunctionOxidative StressReceptors, CholinergicSarcopeniaSuperoxide DismutaseCaspase 3Receptors, CholinergicSod1 protein, mouseSuperoxide DismutaseSuperoxide Dismutase-1Superoxides

Identifiers

PMID20040516
PMCPMC2987499
OpenAlexW2047232246

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.