Evidence map›Paper›PMID 29374361›Full record

ReviewCurrent rheumatology reports2018

Targeting Senescent Cells in Fibrosis: Pathology, Paradox, and Practical Considerations.

Marissa J Schafer, Andrew J Haak, Daniel J Tschumperlin, Nathan K LeBrasseur

Abstract readReview
PubMed Publisher
In one paragraph

Review in Current rheumatology reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 63 papers.

0numbers the graph read from it
0cells of the map it votes in
63citing papers in PubMed
6.4field-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

63 citing papers in PubMed, 95 citations in OpenAlex.

  1. Trial
  2. Magnesium Attenuates Renal Senescence and Fibrosis With Reduced DNA Damage Response and H3K4me3 Enrichment at the p16FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026
    Article
  3. Article
  4. Cellular senescence and aging: molecular mechanisms and convergent pathways.Cellular and molecular life sciences : CMLS · 2026
    Review
  5. Article
  6. Article
  7. Review
  8. Review
  9. Article
  10. Targeting MLL1/WDR5-Mediated Epigenetic Regulation Mitigates Peritoneal Fibrosis by Reducing p16FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025
    Article
  11. Review
  12. Article
  13. Review
  14. Review
  15. Review
  16. Review
  17. Review
  18. Article
  19. Article
  20. Article

3 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.

Marissa J SchaferRobert and Arlene Kogod Center on Aging, Mayo Clinic College of Medicine, 200 First Street SW, Rochester, MN, 55905, USA.
Andrew J HaakDepartment of Physiology and Biomedical Engineering, Mayo Clinic College of Medicine, Rochester, MN, 55905, USA.
Daniel J TschumperlinDepartment of Physiology and Biomedical Engineering, Mayo Clinic College of Medicine, Rochester, MN, 55905, USA.
Nathan K LeBrasseurRobert and Arlene Kogod Center on Aging, Mayo Clinic College of Medicine, 200 First Street SW, Rochester, MN, 55905, USA. lebrasseur.nathan@mayo.edu.
Mayo Clinic · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

purpose of the reviewSenescent cells have the capacity to both effect and limit fibrosis. Senotherapeutics target senescent cells to improve aging conditions. Here, we review the contexts in which senescent cells mediate wound healing and fibrotic pathology and the potential utility of senotherapeutic drugs for treatment of fibrotic disease. RECENT

findingsMulti-action and temporal considerations influence deleterious versus beneficial actions of senescent cells. Acutely generated senescent cells can limit proliferation, and the senescence-associated secretory phenotype (SASP) contains factors that can facilitate tissue repair. Long-lived senescent cells that evade clearance or are generated outside of programmed remodeling can deplete the progenitor pool to exhaust regenerative capacity and through the SASP, stimulate continual activation, leading to disorganized tissue architecture, fibrotic damage, sterile inflammation, and induction of bystander senescence. Senescent cells contribute to fibrotic pathogenesis in multiple tissues, including the liver, kidney, and lung. Senotherapeutics may be a viable strategy for treatment of a range of fibrotic conditions.

Indexed as

AgingAnti-Inflammatory AgentsCellular SenescenceFibrosisHumansScleroderma, SystemicWound HealingAnti-Inflammatory AgentsAgingCellular senescenceFibrosisInflammationSenolyticsSenomorphicsSenotherapeuticsWound healing

Identifiers

PMID29374361
OpenAlexW2792972974

What OpenQuestion holds

Textmetadata
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.