Evidence map›Paper›PMID 34508069›Full record

ReviewBone research2021

Cellular senescence in musculoskeletal homeostasis, diseases, and regeneration.

Mei Wan, Elise F Gray-Gaillard, Jennifer H Elisseeff

Open access · goldAbstract readReview
In one paragraph

Review in Bone research, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 93 papers.

0numbers the graph read from it
0cells of the map it votes in
93citing papers in PubMed
11.2field-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

93 citing papers in PubMed, 132 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Review
  5. Cellular senescence in skeletal muscle regeneration.Cell regeneration (London, England) · 2026
    Review
  6. Article
  7. Review
  8. Article
  9. Article
  10. Review
  11. Cellular Senescence in Skeletal Muscle Aging.Endocrinology and metabolism (Seoul, Korea) · 2026
    Review
  12. Antisense Oligonucleotide Therapeutics Targeting Age-Related Diseases.BioDrugs : clinical immunotherapeutics, biopharmaceuticals and gene therapy · 2026
    Review
  13. ROS Activated NETosis of Bone Marrow CD55Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
    Article
  14. Review
  15. Article
  16. Review
  17. Review
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  19. Review
  20. Article

33 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

3 authors at 1 institution in 1 country.

Mei WanDepartment of Orthopaedic Surgery, The Johns Hopkins University School of Medicine, Baltimore, MD, USA. mwan4@jhmi.edu.ORCID http://orcid.org/0000-0001-9404-540X
Elise F Gray-GaillardTranslational Tissue Engineering Center, Wilmer Eye Institute and the Department of Biomedical Engineering, The Johns Hopkins University, Baltimore, MD, USA.
Jennifer H ElisseeffTranslational Tissue Engineering Center, Wilmer Eye Institute and the Department of Biomedical Engineering, The Johns Hopkins University, Baltimore, MD, USA.ORCID http://orcid.org/0000-0002-5066-1996
Johns Hopkins University · US

Funding

Skeleton and Joint Degeneration with AgingP01AG066603 · NIA · JOHNS HOPKINS UNIVERSITY · PI CAO, XU · 2021 to 2025
$9.2M
Identifying A Skeleton-Derived Factor for Vascular AgingR01AG072090 · NIA · JOHNS HOPKINS UNIVERSITY · PI WAN, MEI · 2021 to 2025
$2.4M
Role of Cellular Senescence in the Bone-Brain InterplayR01AG068226 · NIA · JOHNS HOPKINS UNIVERSITY · PI WAN, MEI · 2020 to 2024
$2.0M
NIA NIH HHS P01 AG066603NIA NIH HHS R01 AG068226NIA NIH HHS R01 AG072090
6 · The paper itself

Abstract

Emerging insights into cellular senescence highlight the relevance of senescence in musculoskeletal disorders, which represent the leading global cause of disability. Cellular senescence was initially described by Hayflick et al. in 1961 as an irreversible nondividing state in in vitro cell culture studies. We now know that cellular senescence can occur in vivo in response to various stressors as a heterogeneous and tissue-specific cell state with a secretome phenotype acquired after the initial growth arrest. In the past two decades, compelling evidence from preclinical models and human data show an accumulation of senescent cells in many components of the musculoskeletal system. Cellular senescence is therefore a defining feature of age-related musculoskeletal disorders, and targeted elimination of these cells has emerged recently as a promising therapeutic approach to ameliorate tissue damage and promote repair and regeneration of the skeleton and skeletal muscles. In this review, we summarize evidence of the role of senescent cells in the maintenance of bone homeostasis during childhood and their contribution to the pathogenesis of chronic musculoskeletal disorders, including osteoporosis, osteoarthritis, and sarcopenia. We highlight the diversity of the senescent cells in the microenvironment of bone, joint, and skeletal muscle tissue, as well as the mechanisms by which these senescent cells are involved in musculoskeletal diseases. In addition, we discuss how identifying and targeting senescent cells might positively affect pathologic progression and musculoskeletal system regeneration.

Identifiers

PMID34508069
PMCPMC8433460
OpenAlexW3197608214

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.