Evidence map›Paper›PMID 34742751›Full record

ReviewMechanisms of ageing and development2021

Skeletal muscle aging, cellular senescence, and senotherapeutics: Current knowledge and future directions.

Davis A Englund, Xu Zhang, Zaira Aversa, Nathan K LeBrasseur

Open access · greenAbstract readReview
In one paragraph

Review in Mechanisms of ageing and development, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 70 papers.

0numbers the graph read from it
0cells of the map it votes in
70citing papers in PubMed
5.5field-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

70 citing papers in PubMed, 79 citations in OpenAlex.

  1. Trial
  2. Article
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  5. Article
  6. Mechanical Loading Induces Distinct and Shared Responses in Endothelial and Muscle Cells and Reveals Exercise-Like Molecular Profiles.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026
    Article
  7. Article
  8. Article
  9. Article
  10. Cellular Senescence in Skeletal Muscle Aging.Endocrinology and metabolism (Seoul, Korea) · 2026
    Review
  11. Article
  12. Does Time Tick Faster in Cerebral Palsy? Accelerated Aging as a Framework for Skeletal Muscle Dysfunction.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026
    Review
  13. Article
  14. Article
  15. Article
  16. Review
  17. Review
  18. Review
  19. Article
  20. Article

10 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.

Davis A EnglundRobert and Arlene Kogod Center on Aging, Mayo Clinic, Rochester, MN, USA; Department of Physical Medicine and Rehabilitation, Mayo Clinic, Rochester, MN, USA.
Xu ZhangRobert and Arlene Kogod Center on Aging, Mayo Clinic, Rochester, MN, USA; Department of Physical Medicine and Rehabilitation, Mayo Clinic, Rochester, MN, USA.
Zaira AversaRobert and Arlene Kogod Center on Aging, Mayo Clinic, Rochester, MN, USA; Department of Physical Medicine and Rehabilitation, Mayo Clinic, Rochester, MN, USA.
Nathan K LeBrasseurRobert and Arlene Kogod Center on Aging, Mayo Clinic, Rochester, MN, USA; Department of Physical Medicine and Rehabilitation, Mayo Clinic, Rochester, MN, USA; Department of Physiology and Biomedical Engineering, Mayo Clinic, Rochester, MN, USA. Electronic address: lebrasseur.nathan@mayo.edu.
Mayo Clinic in Arizona · US

Funding

Targeting Cellular Senescence to Extend HealthspanP01AG062413 · NIA · MAYO CLINIC ROCHESTER · PI Sundeep Khosla · 2019 to 2026
$28.7M
Senescence and Growth Differentiation Factors as Modifiers of AgingR01AG055529 · NIA · MAYO CLINIC ROCHESTER · PI LEBRASSEUR, NATHAN K · 2018 to 2022
$3.1M
Aging and Resiliency in Mice: Optimizing Assessment Protocols and Testing InterventionsR01AG053832 · NIA · MAYO CLINIC ROCHESTER · PI LEBRASSEUR, NATHAN K, MILLER, JORDAN D · 2016 to 2020
$2.0M
Postdoctoral Training Program for Research on AgingT32AG049672 · NIA · MAYO CLINIC ROCHESTER · PI PASSOS, JOAO · 2016 to 2022
$1.3M
Phenotypes of Aging & SenescenceR56AG060907 · NIA · CALIFORNIA PACIFIC MED CTR RES INSTITUTE · PI CUMMINGS, STEVEN RON, LEBRASSEUR, NATHAN K · 2018 to 2018
$684k
NIA NIH HHS P01 AG062413NIA NIH HHS R01 AG053832NIA NIH HHS R01 AG055529NIA NIH HHS R56 AG060907NIA NIH HHS T32 AG049672
6 · The paper itself

Abstract

Cellular senescence is a state of cell cycle arrest induced by several forms of metabolic stress. Senescent cells accumulate with advancing age and have a distinctive phenotype, characterized by profound chromatin alterations and a robust senescence-associated secretory phenotype (SASP) that exerts negative effects on tissue health, both locally and systemically. In preclinical models, pharmacological agents that eliminate senescent cells (senotherapeutics) restore health and youthful properties in multiple tissues. To date, however, very little is understood about the vulnerability of terminally-differentiated skeletal muscle fibers and the resident mononuclear cells that populate the interstitial microenvironment of skeletal muscle to senescence, and their contribution to the onset and progression of skeletal muscle loss and dysfunction with aging. Scientific advances in these areas have the potential to highlight new therapeutic approaches to optimize late-life muscle health. To this end, this review highlights the current evidence and the key questions that need to be addressed to advance the field's understanding of cellular senescence as a mediator of skeletal muscle aging and the potential for emerging senescent cell-targeting therapies to counter age-related deficits in muscle mass, strength, and function. This article is part of the Special Issue - Senolytics - Edited by Joao Passos and Diana Jurk.

Indexed as

Cellular SenescenceMuscle, SkeletalSarcopeniaHumansSenescence-Associated Secretory PhenotypeSenotherapeuticsSenotherapeuticsFibroadipogenic progenitor cellsMuscle fiberSarcopeniaSatellite cellsSenescence-associated secretory phenotypeSenolytics

Identifiers

PMID34742751
PMCPMC8627455
OpenAlexW3208275331

What OpenQuestion holds

Textmetadata
LicenceTDM
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.