Evidence map›Paper›PMID 28729727›Full record

ReviewNature reviews. Drug discovery2017

Senescent cells: an emerging target for diseases of ageing.

Bennett G Childs, Martina Gluscevic, Darren J Baker, Remi-Martin Laberge, Dan Marquess, Jamie Dananberg, Jan M van Deursen

Open access · greenAbstract readReview
In one paragraph

Review in Nature reviews. Drug discovery, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 745 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
745citing papers in PubMed, 1 pooled it
52.1field-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

745 citing papers in PubMed, 1 synthesis or guideline pooled it, 1,186 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Trial
  4. Review
  5. METTL14-Mediated mAging cell · 2026
    Article
  6. Article
  7. Review
  8. Review
  9. Review
  10. 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
  11. Review
  12. Hepatic stellate cells in alcoholic liver cirrhosis: mechanisms of fibrogenesis, plasticity, and fibrosis reversal.Daru : journal of Faculty of Pharmacy, Tehran University of Medical Sciences · 2026
    Review
  13. Senolytics Reverse PMCardiovascular toxicology · 2026
    Article
  14. Article
  15. Article
  16. Senolytic Therapy as a Preventive Strategy for Spine Degeneration and Pain.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
    Article
  17. Review
  18. Article
  19. Article
  20. Article

685 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

7 authors at 3 institutions in 1 country.

Bennett G ChildsDepartments of Biochemistry and Molecular Biology, Mayo Clinic.
Martina GluscevicDepartments of Biochemistry and Molecular Biology, Mayo Clinic.
Darren J BakerDepartments of Biochemistry and Molecular Biology, Mayo Clinic.
Remi-Martin LabergeUnity Biotechnology, 3280 Bayshore Boulevard Suite 100, Brisbane, California 94005, USA.
Dan MarquessUnity Biotechnology, 3280 Bayshore Boulevard Suite 100, Brisbane, California 94005, USA.
Jamie DananbergUnity Biotechnology, 3280 Bayshore Boulevard Suite 100, Brisbane, California 94005, USA.
Jan M van DeursenDepartments of Biochemistry and Molecular Biology, Mayo Clinic.
Mayo Clinic in Arizona · USUnity Biotechnology (United States) · USMayo Clinic in Florida · US

Funding

BUBRI in Normal and Neoplastic GrowthR01CA096985 · NCI · MAYO CLINIC ROCHESTER · PI BAKER, DARREN · 2002 to 2022
$6.2M
Role of PTEN in Chromosome Segregation and its Importance for Tumor SuppressionR01CA168709 · NCI · MAYO CLINIC ROCHESTER · PI VAN DEURSEN, JAN M. · 2012 to 2016
$1.6M
Postdoctoral Training Program for Research on AgingT32AG049672 · NIA · MAYO CLINIC ROCHESTER · PI PASSOS, JOAO · 2016 to 2022
$1.3M
NCI NIH HHS R01 CA096985NCI NIH HHS R01 CA168709NIA NIH HHS T32 AG049672
6 · The paper itself

Abstract

Chronological age represents the single greatest risk factor for human disease. One plausible explanation for this correlation is that mechanisms that drive ageing might also promote age-related diseases. Cellular senescence, which is a permanent state of cell cycle arrest induced by cellular stress, has recently emerged as a fundamental ageing mechanism that also contributes to diseases of late life, including cancer, atherosclerosis and osteoarthritis. Therapeutic strategies that safely interfere with the detrimental effects of cellular senescence, such as the selective elimination of senescent cells (SNCs) or the disruption of the SNC secretome, are gaining significant attention, with several programmes now nearing human clinical studies.

Indexed as

AgingAnimalsAtherosclerosisCell Cycle CheckpointsCell ProliferationCellular SenescenceHumansNeoplasms

Identifiers

PMID28729727
PMCPMC5942225
OpenAlexW2739438570

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.