Evidence map›Paper›PMID 32997601›Full record

ReviewAnnual review of pharmacology and toxicology2021

Senolytic Drugs: Reducing Senescent Cell Viability to Extend Health Span.

Paul D Robbins, Diana Jurk, Sundeep Khosla, James L Kirkland, Nathan K LeBrasseur, Jordan D Miller, João F Passos, Robert J Pignolo, Tamar Tchkonia, Laura J Niedernhofer

Open access · bronzeAbstract readReview
In one paragraph

Review in Annual review of pharmacology and toxicology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 195 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
195citing papers in PubMed, 1 pooled it
17.9field-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

195 citing papers in PubMed, 1 synthesis or guideline pooled it, 296 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Review
  4. Article
  5. Review
  6. Life (Basel, Switzerland) · 2026
    Review
  7. Article
  8. Review
  9. Article
  10. Review
  11. Targeting cellular senescence alleviates bone marrow aging.bioRxiv : the preprint server for biology · 2026
    Article
  12. Cellular senescence and aging: molecular mechanisms and convergent pathways.Cellular and molecular life sciences : CMLS · 2026
    Review
  13. Review
  14. Article
  15. Review
  16. Article
  17. Article
  18. The Aging Kidney and Acute Kidney Injury.Journal of the American Society of Nephrology : JASN · 2026
    Review
  19. Article
  20. Review

135 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

10 authors at 2 institutions in 1 country.

Paul D RobbinsInstitute on the Biology of Aging and Metabolism, Department of Biochemistry, Molecular Biology and Biophysics, University of Minnesota Medical School, Minneapolis, Minnesota 55455, USA; email: lniedern@umn.edu.
Diana JurkRobert and Arlene Kogod Center on Aging, Mayo Clinic, Rochester, Minnesota 55905, USA.
Sundeep KhoslaRobert and Arlene Kogod Center on Aging, Mayo Clinic, Rochester, Minnesota 55905, USA.
James L KirklandRobert and Arlene Kogod Center on Aging, Mayo Clinic, Rochester, Minnesota 55905, USA.
Nathan K LeBrasseurRobert and Arlene Kogod Center on Aging, Mayo Clinic, Rochester, Minnesota 55905, USA.
Jordan D MillerRobert and Arlene Kogod Center on Aging, Mayo Clinic, Rochester, Minnesota 55905, USA.
João F PassosRobert and Arlene Kogod Center on Aging, Mayo Clinic, Rochester, Minnesota 55905, USA.
Robert J PignoloRobert and Arlene Kogod Center on Aging, Mayo Clinic, Rochester, Minnesota 55905, USA.
Tamar TchkoniaRobert and Arlene Kogod Center on Aging, Mayo Clinic, Rochester, Minnesota 55905, USA.
Laura J NiedernhoferInstitute on the Biology of Aging and Metabolism, Department of Biochemistry, Molecular Biology and Biophysics, University of Minnesota Medical School, Minneapolis, Minnesota 55455, USA; email: lniedern@umn.edu.
Mayo Clinic in Florida · USUniversity of Minnesota · US

Funding

Targeting Cellular Senescence to Extend HealthspanP01AG062413 · NIA · MAYO CLINIC ROCHESTER · PI Sundeep Khosla · 2019 to 2026
$28.7M
Validation and characterization of the identified variants associated with human longevity in mouse modelsU19AG056278 · NIA · ALBERT EINSTEIN COLLEGE OF MEDICINE, INC · PI JAN VIJG · 2017 to 2026
$24.5M
PROTEOMICSP01AG043376 · NIA · UNIVERSITY OF MINNESOTA · PI ROBBINS, PAUL D. · 2013 to 2019
$11.2M
Effect of Aging on Preadipocyte DifferentiationR37AG013925 · NIA · MAYO CLINIC ROCHESTER · PI KIRKLAND, JAMES L. · 2016 to 2025
$6.6M
Using the senolytic fisetin to suppress mortality in aged mice acutely exposed to murine beta-coronavirusR01AG063543 · NIA · UNIVERSITY OF MINNESOTA · PI NIEDERNHOFER, LAURA JANE · 2019 to 2023
$3.4M
The role of sub-lethal mitochondrial apoptotic stress in cellular senescenceR01AG068048 · NIA · MAYO CLINIC ROCHESTER · PI PASSOS, JOAO · 2020 to 2024
$2.2M
Development of machine learning software to quantitatively map telomere induced senescence in tissue sections during agingUG3CA268103 · NCI · MAYO CLINIC ROCHESTER · PI PASSOS, JOAO · 2021 to 2022
$1.1M
Extracellular vesicles as cell non-autonomous geronic factorsR56AG059675 · NIA · UNIVERSITY OF MINNESOTA · PI ROBBINS, PAUL D. · 2018 to 2018
$385k
Immune cells as a driver of cell non-autonomous agingR56AG059676 · NIA · UNIVERSITY OF MINNESOTA · PI NIEDERNHOFER, LAURA JANE · 2018 to 2018
$385k
NCI NIH HHS UG3 CA268103NIA NIH HHS P01 AG043376NIA NIH HHS P01 AG062413NIA NIH HHS R01 AG063543NIA NIH HHS R01 AG068048NIA NIH HHS R37 AG013925NIA NIH HHS R56 AG059675NIA NIH HHS R56 AG059676NIA NIH HHS U19 AG056278
6 · The paper itself

Abstract

Senescence is the consequence of a signaling mechanism activated in stressed cells to prevent proliferation of cells with damage. Senescent cells (Sncs) often develop a senescence-associated secretory phenotype to prompt immune clearance, which drives chronic sterile inflammation and plays a causal role in aging and age-related diseases. Sncs accumulate with age and at anatomical sites of disease. Thus, they are regarded as a logical therapeutic target. Senotherapeutics are a new class of drugs that selectively kill Sncs (senolytics) or suppress their disease-causing phenotypes (senomorphics/senostatics). Since 2015, several senolytics went from identification to clinical trial. Preclinical data indicate that senolytics alleviate disease in numerous organs, improve physical function and resilience, and suppress all causes of mortality, even if administered to the aged. Here, we review the evidence that Sncs drive aging and disease, the approaches to identify and optimize senotherapeutics, and the current status of preclinical and clinical testing of senolytics.

Indexed as

Cellular SenescencePharmaceutical PreparationsAgedAgingHumansPhenotypeSignal TransductionPharmaceutical Preparationsagingsenescencesenescence-associated secretory phenotypesenolyticssenomorphics

Identifiers

PMID32997601
PMCPMC7790861
OpenAlexW3089880422

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.