Evidence map›Paper›PMID 35903886›Full record

ReviewConnective tissue research2023

Impact of aging on tendon homeostasis, tendinopathy development, and impaired healing.

Antonion Korcari, Samantha J Przybelski, Anne Gingery, Alayna E Loiselle

Open access · greenAbstract readReview
In one paragraph

Review in Connective tissue research, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
6.8field-weighted citation impact, top 2% 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

30 citing papers in PubMed, 39 citations in OpenAlex.

  1. Trial
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  5. Article
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  10. Review
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  13. Ginsenoside Rg5 mitigates tenocyte deathJournal of ginseng research · 2026
    Article
  14. Review
  15. Article
  16. Review
  17. Article
  18. Loss ofMatrix biology plus · 2025
    Article
  19. Fluoroquinolone-Mediated Tendinopathy and Tendon Rupture.Pharmaceuticals (Basel, Switzerland) · 2025
    Review
  20. Article
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 2 institutions in 1 country.

Antonion KorcariDepartment of Orthopaedics & Rehabilitation, Center for Musculoskeletal Research, University of Rochester Medical Center, Rochester, NY, USA.ORCID 0000-0002-5964-5212
Samantha J PrzybelskiDivision of Orthopedic Surgery Research, Mayo Clinic, Rochester, MN, USA.
Anne GingeryDivision of Orthopedic Surgery Research, Mayo Clinic, Rochester, MN, USA.
Alayna E LoiselleDepartment of Orthopaedics & Rehabilitation, Center for Musculoskeletal Research, University of Rochester Medical Center, Rochester, NY, USA.
Mayo Clinic in Arizona · USUniversity of Rochester Medical Center · US

Funding

The Role of Cellular Senescence in Carpal Tunnel Syndrome.R01AR076347 · NIAMS · MAYO CLINIC ROCHESTER · PI Anne Gingery · 2020 to 2026
$3.3M
Modulating Cell-fate to Promote Regenerative Tendon HealingR01AR077527 · NIAMS · UNIVERSITY OF ROCHESTER · PI LOISELLE, ALAYNA · 2021 to 2025
$2.0M
s100a4 Signaling in Fibrotic Diabetic Tendon HealingR01AR073169 · NIAMS · UNIVERSITY OF ROCHESTER · PI LOISELLE, ALAYNA · 2018 to 2022
$1.7M
NIAMS NIH HHS R01 AR073169NIAMS NIH HHS R01 AR076347NIAMS NIH HHS R01 AR077527
6 · The paper itself

Abstract

Aging is a complex and progressive process where the tissues of the body demonstrate a decreased ability to maintain homeostasis. During aging, there are substantial cellular and molecular changes, with a subsequent increase in susceptibility to pathological degeneration of normal tissue function. In tendon, aging results in well characterized alterations in extracellular matrix (ECM) structure and composition. In addition, the cellular environment of aged tendons is altered, including a marked decrease in cell density and metabolic activity, as well as an increase in cellular senescence. Collectively, these degenerative changes make aging a key risk factor for the development of tendinopathies and can increase the frequency of tendon injuries. However, inconsistencies in the extent of age-related degenerative impairments in tendons have been reported, likely due to differences in how "old" and "young" age-groups have been defined, differences between anatomically distinct tendons, and differences between animal models that have been utilized to study the impact of aging on tendon homeostasis. In this review, we address these issues by summarizing data by well-defined age categories (young adults, middle-aged, and aged) and from anatomically distinct tendon types. We then summarize in detail how aging affects tendon mechanics, structure, composition, and the cellular environment based on current data and underscore what is currently not known. Finally, we discuss gaps in the current understanding of tendon aging and propose key avenues for future research that can shed light on the specific mechanisms of tendon pathogenesis due to aging.

Indexed as

TendinopathyTendon InjuriesAgingAnimalsHomeostasisTendonsagingextracellular matrixtendinopathyTendontendon healing

Identifiers

PMID35903886
PMCPMC9851966
OpenAlexW4288491042

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.