Evidence map›Paper›PMID 33511781›Full record

ArticleAging cell2021

Delineating the relationship between immune system aging and myogenesis in muscle repair.

Stephanie W Tobin, Faisal J Alibhai, Lukasz Wlodarek, Azadeh Yeganeh, Sean Millar, Jun Wu, Shu-Hong Li, Richard D Weisel, Ren-Ke Li

Open access · goldAbstract read
In one paragraph

Article in Aging cell, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
2.1field-weighted citation impact, top 12% 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

28 citing papers in PubMed, 37 citations in OpenAlex.

  1. Review
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  7. Molecular Framework of the Onset and Progression of Skeletal Muscle Aging.International journal of molecular sciences · 2025
    Review
  8. Article
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  17. Macrophage senescence in health and diseases.Acta pharmaceutica Sinica. B · 2024
    Review
  18. Article
  19. Article
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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

9 authors at 1 institution in 1 country.

Stephanie W TobinDivision of Cardiovascular Surgery, Toronto General Research Institute, University Health Network, Toronto, ON, Canada.
Faisal J AlibhaiDivision of Cardiovascular Surgery, Toronto General Research Institute, University Health Network, Toronto, ON, Canada.
Lukasz WlodarekDivision of Cardiovascular Surgery, Toronto General Research Institute, University Health Network, Toronto, ON, Canada.
Azadeh YeganehDivision of Cardiovascular Surgery, Toronto General Research Institute, University Health Network, Toronto, ON, Canada.
Sean MillarDivision of Cardiovascular Surgery, Toronto General Research Institute, University Health Network, Toronto, ON, Canada.
Jun WuDivision of Cardiovascular Surgery, Toronto General Research Institute, University Health Network, Toronto, ON, Canada.
Shu-Hong LiDivision of Cardiovascular Surgery, Toronto General Research Institute, University Health Network, Toronto, ON, Canada.
Richard D WeiselDivision of Cardiovascular Surgery, Toronto General Research Institute, University Health Network, Toronto, ON, Canada.
Ren-Ke LiDivision of Cardiovascular Surgery, Toronto General Research Institute, University Health Network, Toronto, ON, Canada.ORCID 0000-0002-2584-060X
University Health Network · CA

Funding

CIHR 332652
6 · The paper itself

Abstract

Recruited immune cells play a critical role in muscle repair, in part by interacting with local stem cell populations to regulate muscle regeneration. How aging affects their communication during myogenesis is unclear. Here, we investigate how aging impacts the cellular function of these two cell types after muscle injury during normal aging or after immune rejuvenation using a young to old (Y-O) or old to old (O-O) bone marrow (BM) transplant model. We found that skeletal muscle from old mice (20 months) exhibited elevated basal inflammation and possessed fewer satellite cells compared with young mice (3 months). After cardiotoxin muscle injury (CTX), old mice exhibited a blunted inflammatory response compared with young mice and enhanced M2 macrophage recruitment and IL-10 expression. Temporal immune and cytokine responses of old mice were partially restored to a young phenotype following reconstitution with young cells (Y-O chimeras). Improved immune responses in Y-O chimeras were associated with greater satellite cell proliferation compared with O-O chimeras. To identify how immune cell aging affects myoblast function, conditioned media (CM) from activated young or old macrophages was applied to cultured C2C12 myoblasts. CM from young macrophages inhibited myogenesis while CM from old macrophages reduced proliferation. These functional differences coincided with age-related differences in macrophage cytokine expression. Together, this study examines the infiltration and proliferation of immune cells and satellite cells after injury in the context of aging and, using BM chimeras, demonstrates that young immune cells retain cell autonomy in an old host to increase satellite cell proliferation.

Indexed as

AnimalsCardiotoxinsCellular SenescenceMiceMuscle DevelopmentSatellite Cells, Skeletal MuscleCardiotoxinsagingbone marrow transplantinflammationmyogenesissatellite cells

Identifiers

PMID33511781
PMCPMC7884032
OpenAlexW3124244005

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.