Evidence map›Paper›PMID 36116755›Full record

ReviewMolecular metabolism2022

Targeting cellular senescence in metabolic disease.

Allyson K Palmer, Tamar Tchkonia, James L Kirkland

Open access · goldAbstract readReview
In one paragraph

Review in Molecular metabolism, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.

0numbers the graph read from it
0cells of the map it votes in
42citing papers in PubMed
7.1field-weighted citation impact, top 2% 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

42 citing papers in PubMed, 65 citations in OpenAlex.

  1. Article
  2. Article
  3. Centriolar Protein POC5 Regulates Human Adipogenesis and Cellular Senescence: Insights From a Novel Metabolic Ciliopathy.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026
    Article
  4. Review
  5. Article
  6. Review
  7. Article
  8. Review
  9. Review
  10. Article
  11. Article
  12. Review
  13. Article
  14. Review
  15. Review
  16. Review
  17. Review
  18. Article
  19. Aging · 2025
    Article
  20. The states of senescent cells.Biochemical Society transactions · 2025
    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

3 authors at 1 institution in 1 country.

Allyson K PalmerDivision of Hospital Internal Medicine, Mayo Clinic, 200 1st Street SW, Rochester, MN, 55905, USA; Robert and Arlene Kogod Center on Aging, Mayo Clinic, 200 1st Street SW, Rochester, MN, 55905, USA.
Tamar TchkoniaDepartment of Physiology and Biomedical Engineering, Mayo Clinic, 200 1st Street SW, Rochester, MN, 55905, USA.
James L KirklandDepartment of Physiology and Biomedical Engineering, Mayo Clinic, 200 1st Street SW, Rochester, MN, 55905, USA; Division of General Internal Medicine, Mayo Clinic, 200 1st Street SW, Rochester, MN, 55905, USA. Electronic address: Kirkland.james@mayo.edu.
Mayo Clinic · US

Funding

Targeting Cellular Senescence to Extend HealthspanP01AG062413 · NIA · MAYO CLINIC ROCHESTER · PI Sundeep Khosla, Nathan K LeBrasseur · 2019 to 2026
$28.7M
Effect of Aging on Preadipocyte DifferentiationR37AG013925 · NIA · MAYO CLINIC ROCHESTER · PI KIRKLAND, JAMES L. · 2016 to 2025
$6.6M
Translational Geroscience NetworkR33AG061456 · NIA · MAYO CLINIC ROCHESTER · PI JAMES L. KIRKLAND, STEPHEN B. KRITCHEVSKY · 2019 to 2026
$6.2M
Obesity-induced mesenchymal stem cell senescenceR01DK120292 · NIDDK · MAYO CLINIC ROCHESTER · PI LERMAN, LILACH O · 2019 to 2022
$2.6M
COVID-FIS: A PHASE 2 PLACEBO-CONTROLLED PILOT STUDY IN COVID-19 OF FISETIN TO ALLEVIATE DYSFUNCTION AND EXCESSIVE INFLAMMATORY RESPONSE IN OLDER ADULTS IN NURSING HOMESR01AG072301 · NIA · MAYO CLINIC ROCHESTER · PI PIGNOLO, ROBERT JOHN · 2020 to 2024
$1.9M
NIA NIH HHS P01 AG062413NIA NIH HHS R01 AG072301NIA NIH HHS R33 AG061456NIA NIH HHS R37 AG013925NIDDK NIH HHS R01 DK120292
6 · The paper itself

Abstract

Cellular senescence is a cell fate involving cell cycle arrest, resistance against apoptosis, and the development of a secretome that can be pro-inflammatory. In aging and obesity, senescent cells accumulate in many tissues, including adipose tissue, brain, kidney, pancreas, and liver. These senescent cells and their downstream effects appear to perpetuate inflammation and have been implicated in the pathogenesis of metabolic dysfunction. Senescent cells are cleared in part by the immune system, a process that is diminished in obesity and aging, likely due in part to senescence of immune cells themselves. Targeting senescent cells or their products improves metabolic function in both aging and in animal models of obesity. Novel therapeutics to target senescent cells are on the horizon and are currently being investigated in clinical trials in humans for multiple diseases. Early evidence suggests that senolytic drugs, which transiently disarm the anti-apoptotic defenses of pro-inflammatory senescent cells, are effective in causing depletion of senescent cells in humans. Senescence-targeting therapeutics, including senolytic drugs and strategies to increase immune clearance of senescent cells, hold significant promise for treating metabolic dysfunction in multiple tissues and disease states.

Indexed as

Metabolic DiseasesSenotherapeuticsAgingAnimalsCellular SenescenceHumansObesitySenotherapeuticsAdiposeAgingCellular senescenceObesitySenolytics

Identifiers

PMID36116755
PMCPMC9520013
OpenAlexW4296050459

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.