Evidence map›Paper›PMID 28416161›Full record

ReviewEBioMedicine2017

Cellular Senescence: A Translational Perspective.

James L Kirkland, Tamara Tchkonia

Open access · goldAbstract readReview
In one paragraph

Review in EBioMedicine, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 611 papers.

0numbers the graph read from it
0cells of the map it votes in
611citing papers in PubMed
48.1field-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

611 citing papers in PubMed, 962 citations in OpenAlex.

  1. Trial
  2. Biomarkers of Cellular Senescence Predict the Onset of Mobility Disability and Are Reduced by Physical Activity in Older Adults.The journals of gerontology. Series A, Biological sciences and medical sciences · 2024
    Trial
  3. Article
  4. Article
  5. Tyrosine kinase inhibitor use and risk of neurodegenerative disease: A Swedish population-based cohort study.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026
    Article
  6. Article
  7. Review
  8. Article
  9. Age-associated Autoimmunity Driven by T cell Immunosenescence.bioRxiv : the preprint server for biology · 2026
    Article
  10. Article
  11. Review
  12. Review
  13. Review
  14. Review
  15. 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
  16. Article
  17. Article
  18. Senolytic Therapy as a Preventive Strategy for Spine Degeneration and Pain.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
    Article
  19. Review
  20. Review

551 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

2 authors at 1 institution in 1 country.

James L KirklandRobert and Arlene Kogod Center on Aging, Mayo Clinic, Rochester, MN, United States. Electronic address: kirkland.james@mayo.edu.
Tamara TchkoniaRobert and Arlene Kogod Center on Aging, Mayo Clinic, Rochester, MN, United States.
Mayo Clinic in Florida · US

Funding

Effect of Aging on Preadipocyte DifferentiationR37AG013925 · NIA · MAYO CLINIC ROCHESTER · PI KIRKLAND, JAMES L. · 2016 to 2025
$6.6M
Effect of Aging on Preadipocyte DifferentiationR01AG013925 · NIA · MAYO CLINIC ROCHESTER · PI KIRKLAND, JAMES L. · 1997 to 2012
$3.7M
NIA NIH HHS R01 AG013925NIA NIH HHS R37 AG013925
6 · The paper itself

Abstract

Cellular senescence entails essentially irreversible replicative arrest, apoptosis resistance, and frequently acquisition of a pro-inflammatory, tissue-destructive senescence-associated secretory phenotype (SASP). Senescent cells accumulate in various tissues with aging and at sites of pathogenesis in many chronic diseases and conditions. The SASP can contribute to senescence-related inflammation, metabolic dysregulation, stem cell dysfunction, aging phenotypes, chronic diseases, geriatric syndromes, and loss of resilience. Delaying senescent cell accumulation or reducing senescent cell burden is associated with delay, prevention, or alleviation of multiple senescence-associated conditions. We used a hypothesis-driven approach to discover pro-survival Senescent Cell Anti-apoptotic Pathways (SCAPs) and, based on these SCAPs, the first senolytic agents, drugs that cause senescent cells to become susceptible to their own pro-apoptotic microenvironment. Several senolytic agents, which appear to alleviate multiple senescence-related phenotypes in pre-clinical models, are beginning the process of being translated into clinical interventions that could be transformative.

Indexed as

AgingAnimal ExperimentationAnimalsApoptosisBiomarkersCellular SenescenceChronic DiseaseDisease SusceptibilityDrug DiscoveryHumansPhenotypeSecretory PathwaySignal TransductionTranslational Research, BiomedicalBiomarkersA1155463A1331852DasatinibFisetinNavitoclaxQuercetinSASP inhibitorsSenescent Cell Anti-apoptotic Pathways (SCAPs)Senolytics

Identifiers

PMID28416161
PMCPMC5514381
OpenAlexW2605674430

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.