Evidence map›Paper›PMID 26009878›Full record

ArticleAging cell2015

Increases of M2a macrophages and fibrosis in aging muscle are influenced by bone marrow aging and negatively regulated by muscle-derived nitric oxide.

Ying Wang, Michelle Wehling-Henricks, Giuseppina Samengo, James G Tidball

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Aging cell, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 141 papers.

0numbers the graph read from it
0cells of the map it votes in
141citing papers in PubMed
12.3field-weighted citation impact, top 1% 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

141 citing papers in PubMed, 196 citations in OpenAlex.

  1. Neuromuscular electrical stimulation and protein during bed rest increases CD11bApplied physiology, nutrition, and metabolism = Physiologie appliquee, nutrition et metabolisme · 2020
    Trial
  2. Trial
  3. Article
  4. Article
  5. Article
  6. Review
  7. Review
  8. Deletion of Tgf-β1 From CD206Journal of cachexia, sarcopenia and muscle · 2026
    Article
  9. Review
  10. Review
  11. Article
  12. Review
  13. Article
  14. Article
  15. Review
  16. Article
  17. Review
  18. Review
  19. Review
  20. Review

81 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

4 authors at 1 institution in 1 country.

Ying WangMolecular, Cellular & Integrative Physiology Program, University of California, Los Angeles, CA, 90095, USA.
Michelle Wehling-HenricksDepartment of Integrative Biology and Physiology, University of California, Los Angeles, CA, 90095, USA.
Giuseppina SamengoDepartment of Integrative Biology and Physiology, University of California, Los Angeles, CA, 90095, USA.
James G TidballMolecular, Cellular & Integrative Physiology Program, University of California, Los Angeles, CA, 90095, USA.
University of California, Los Angeles · US

Funding

Regulation of sarcopenia and muscle dysfunction by nitric oxideR01AR054451 · NIAMS · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI TIDBALL, JAMES G · 2007 to 2011
$1.8M
Functions of myelomonocytic lineage cells in aging muscleR01AG041147 · NIA · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI TIDBALL, JAMES G · 2011 to 2015
$1.7M
NIAMS NIH HHS R01 AR054451NIAMS NIH HHS R01AR054451NIA NIH HHS R01 AG041147NIA NIH HHS R01AG041147
6 · The paper itself

Abstract

Muscle aging is associated with changes in myeloid cell phenotype that may influence age-related changes in muscle structure. We tested whether preventing age-related reductions in muscle neuronal nitric oxide synthase (nNOS) would obviate age-related changes in myeloid cells in muscle. Our findings show that muscle aging is associated with elevations of anti-inflammatory M2a macrophages that can increase muscle fibrosis. Expression of a muscle-specific nNOS transgene in mice prevented age-related increases in M2a macrophages. Transgene expression also reduced expression of collagens and decreased muscle fibrosis. The nNOS transgene prevented age-related increases in arginase-1 but did not influence TGFβ expression, indicating that the transgene may prevent age-related muscle fibrosis by inhibiting the arginase-dependent profibrotic pathway. Although aged satellite cells or fibro-adipogenic precursor (FAPs) cells also promote fibrosis, transgene expression had no effect on the expression of key signaling molecules that regulate fibrogenic activity of those cells. Finally, we tested whether increases in M2a macrophages and the associated increase in fibrosis were attributable to aging of myeloid lineage cells. Young bone marrow cells (BMCs) were transplanted into young or old mice, and muscles were collected 8 months later. Muscles of young mice receiving young BMCs showed no effect on M2a macrophage number or collagen accumulation compared to age-matched, nontransplanted controls. However, muscles of old mice receiving young BMCs showed fewer M2a macrophages and less accumulation of collagen. Thus, the age-related increase in M2a macrophages in aging muscle and the associated muscle fibrosis are determined in part by the age of bone marrow cells.

Indexed as

AgingAnimalsArginaseBone Marrow CellsCell CountCollagenFemaleFibrosisGene Expression Regulation, DevelopmentalHumansMacrophagesMaleMiceMice, TransgenicMuscle, SkeletalNeuronsArg1 protein, mouseArginaseCollagenNitric OxideNitric Oxide Synthase Type INos1 protein, mouseTransforming Growth Factor betaagingfibrosisinflammationmacrophagemousenitric oxide synthaseskeletal muscle

Identifiers

PMID26009878
PMCPMC4531081
OpenAlexW1539477086

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.