Evidence map›Paper›PMID 34363464›Full record

ReviewEndocrinology2021

Role of Cellular Senescence in Type II Diabetes.

Akilavalli Narasimhan, Rafael R Flores, Paul D Robbins, Laura J Niedernhofer

Open access · bronzeAbstract readReview
In one paragraph

Review in Endocrinology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 65 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
65citing papers in PubMed, 1 pooled it
8.6field-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

65 citing papers in PubMed, 1 synthesis or guideline pooled it, 121 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Review
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  5. Article
  6. Review
  7. Review
  8. Review
  9. Article
  10. Article
  11. Article
  12. Pleiotropic regulatory mechanisms and targeted therapeutic prospects of Galectin-3 in aging-related diseases.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2025
    Review
  13. Article
  14. Review
  15. How to measure and model cardiovascular aging.Cardiovascular research · 2025
    Review
  16. Article
  17. Article
  18. High-Fat Diet Disrupt Nerve Function by Targeting Schwann Cells.Journal of the peripheral nervous system : JPNS · 2025
    Article
  19. Review
  20. Review

5 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.

Akilavalli NarasimhanInstitute on the Biology of Aging and Metabolism, Department of Biochemistry, Molecular Biology, and Biophysics, University of Minnesota Medical School, 55455, USA.
Rafael R FloresInstitute on the Biology of Aging and Metabolism, Department of Biochemistry, Molecular Biology, and Biophysics, University of Minnesota Medical School, 55455, USA.
Paul D RobbinsInstitute on the Biology of Aging and Metabolism, Department of Biochemistry, Molecular Biology, and Biophysics, University of Minnesota Medical School, 55455, USA.ORCID 0000-0003-1068-7099
Laura J NiedernhoferInstitute on the Biology of Aging and Metabolism, Department of Biochemistry, Molecular Biology, and Biophysics, University of Minnesota Medical School, 55455, USA.ORCID 0000-0002-5580-6381
University of Minnesota · US

Funding

Targeting Cellular Senescence to Extend HealthspanP01AG062413 · NIA · MAYO CLINIC ROCHESTER · PI Sundeep Khosla, Nathan K LeBrasseur · 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 NIR J BARZILAI, Paul D. Robbins · 2017 to 2026
$24.5M
PROTEOMICSP01AG043376 · NIA · UNIVERSITY OF MINNESOTA · PI ROBBINS, PAUL D. · 2013 to 2019
$11.2M
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
NIA NIH HHS P01 AG043376NIA NIH HHS P01 AG062413NIA NIH HHS R01 AG063543NIA NIH HHS U19 AG056278
6 · The paper itself

Abstract

Cellular senescence is a cell fate that occurs in response to numerous types of stress and can promote tissue repair or drive inflammation and disruption of tissue homeostasis depending on the context. Aging and obesity lead to an increase in the senescent cell burden in multiple organs. Senescent cells release a myriad of senescence-associated secretory phenotype factors that directly mediate pancreatic β-cell dysfunction, adipose tissue dysfunction, and insulin resistance in peripheral tissues, which promote the onset of type II diabetes mellitus. In addition, hyperglycemia and metabolic changes seen in diabetes promote cellular senescence. Diabetes-induced cellular senescence contributes to various diabetic complications. Thus, type II diabetes is both a cause and consequence of cellular senescence. This review summarizes recent studies on the link between aging, obesity, and diabetes, focusing on the role of cellular senescence in disease processes.

Indexed as

Cellular SenescenceAdipose TissueAgingAnimalsCardiovascular DiseasesDiabetes Mellitus, Type 2Diabetic NephropathiesDiabetic RetinopathyDisease Models, AnimalHumansHyperglycemiaImmune SystemInflammationInsulinInsulin ResistanceInsulin-Secreting CellsInsulinMTOR protein, humanTOR Serine-Threonine Kinasesagingcellular senescenceDiabetesinflammationobesitysenotherapeutics

Identifiers

PMID34363464
PMCPMC8386762
OpenAlexW3188031952

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.