Evidence map›Paper›PMID 25447026›Full record

ArticleStem cells (Dayton, Ohio)2015

Age-specific functional epigenetic changes in p21 and p16 in injury-activated satellite cells.

Ju Li, Suhyoun Han, Wendy Cousin, Irina M Conboy

Open access · bronzeAbstract read
In one paragraph

Article in Stem cells (Dayton, Ohio), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
1.7field-weighted citation impact, top 16% 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

33 citing papers in PubMed, 51 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. The impact of cellular senescence on aging skeletal muscle.Frontiers in cell and developmental biology · 2025
    Review
  5. Article
  6. Article
  7. Review
  8. Article
  9. Review
  10. Article
  11. Article
  12. Review
  13. Review
  14. FGF-2-dependent signaling activated in aged human skeletal muscle promotes intramuscular adipogenesis.Proceedings of the National Academy of Sciences of the United States of America · 2021
    Article
  15. Article
  16. FGF/FGFR signaling in health and disease.Signal transduction and targeted therapy · 2020
    Review
  17. Article
  18. Review
  19. The eroding chromatin landscape of aging stem cells.Translational medicine of aging · 2020
    Article
  20. Review
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.

Ju LiDepartment of Bioengineering, University of California-Berkeley, Berkeley, California, USA; California Institute for Quantitative Biosciences (QB3), Berkeley, California, USA.
Suhyoun Han
Wendy Cousin
Irina M Conboy
QB3 · USUniversity of California, Berkeley · US

Funding

Effects of the systemic environment on muscle agingR01AG027252 · NIA · UNIVERSITY OF CALIFORNIA BERKELEY · PI CONBOY, IRINA M · 2007 to 2012
$1.7M
NIA NIH HHS R01 AG027252NIA NIH HHS R01 AG02725201
6 · The paper itself

Abstract

The regenerative capacity of muscle dramatically decreases with age because old muscle stem cells fail to proliferate in response to tissue damage. Here, we uncover key age-specific differences underlying this proliferative decline: namely, the genetic loci of cyclin/cyclin-dependent kinase (CDK) inhibitors (CDKIs) p21 and p16 are more epigenetically silenced in young muscle stem cells, as compared to old, both in quiescent cells and those responding to tissue injury. Interestingly, phosphorylated ERK (pERK) induced in these cells by ectopic FGF2 is found in association with p21 and p16 promoters, and moreover, only in the old cells. Importantly, in the old satellite cells, FGF2/pERK silences p21 epigenetically and transcriptionally, which leads to reduced p21 protein levels and enhanced cell proliferation. In agreement with the epigenetic silencing of the loci, young muscle stem cells do not depend as much as old on ectopic FGF/pERK for their myogenic proliferation. In addition, other CDKIs, such asp15(INK4B) and p27(KIP1) , become elevated in satellite cells with age, confirming and explaining the profound regenerative defect of old muscle. This work enhances our understanding of tissue aging, promoting strategies for combating age-imposed tissue degeneration.

Indexed as

Age FactorsAnimalsCyclin-Dependent Kinase Inhibitor p16Cyclin-Dependent Kinase Inhibitor p21Epigenesis, GeneticGuided Tissue RegenerationMiceMice, Inbred C57BLMuscle, SkeletalSatellite Cells, Skeletal MuscleSignal TransductionCyclin-Dependent Kinase Inhibitor p16Cyclin-Dependent Kinase Inhibitor p21AgingCDK inhibitorChromatinEpigeneticMAPKMuscle stem cellspERKSignal transductionTissue regeneration

Identifiers

PMID25447026
PMCPMC4333004
OpenAlexW2102525221

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.