Evidence map›Paper›PMID 26106186›Full record

ReviewDiabetes2015

Cellular Senescence in Type 2 Diabetes: A Therapeutic Opportunity.

Allyson K Palmer, Tamara Tchkonia, Nathan K LeBrasseur, Eduardo N Chini, Ming Xu, James L Kirkland

Open access · bronzeAbstract readReview
In one paragraph

Review in Diabetes, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 249 papers.

0numbers the graph read from it
0cells of the map it votes in
249citing papers in PubMed
14.1field-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

249 citing papers in PubMed, 403 citations in OpenAlex.

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189 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

6 authors at 1 institution in 1 country.

Allyson K PalmerRobert and Arlene Kogod Center on Aging, Mayo Clinic, Rochester, MN Mayo Medical Scientist Training Program, Mayo Graduate School, Mayo Medical School, Rochester, MN.
Tamara TchkoniaRobert and Arlene Kogod Center on Aging, Mayo Clinic, Rochester, MN.
Nathan K LeBrasseurRobert and Arlene Kogod Center on Aging, Mayo Clinic, Rochester, MN.
Eduardo N ChiniRobert and Arlene Kogod Center on Aging, Mayo Clinic, Rochester, MN Department of Anesthesiology, Mayo Clinic, Rochester, MN.
Ming XuRobert and Arlene Kogod Center on Aging, Mayo Clinic, Rochester, MN.
James L KirklandRobert and Arlene Kogod Center on Aging, Mayo Clinic, Rochester, MN kirkland.james@mayo.edu.
Mayo Clinic · US

Funding

Systems Biology and Bioinformatics CoreP01AG041122 · NIA · MAYO CLINIC ROCHESTER · PI CAMPISI, JUDITH · 2012 to 2016
$9.8M
Effect of Aging on Preadipocyte DifferentiationR37AG013925 · NIA · MAYO CLINIC ROCHESTER · PI KIRKLAND, JAMES L. · 2016 to 2025
$6.6M
The Sir2-p53-IGF Link in Mammalian Life-Span ControlR01AG026094 · NIA · UNIVERSITY OF VIRGINIA · PI CHINI, EDUARDO N · 2006 to 2016
$3.8M
Effect of Aging on Preadipocyte DifferentiationR01AG013925 · NIA · MAYO CLINIC ROCHESTER · PI KIRKLAND, JAMES L. · 1997 to 2012
$3.7M
Geroscience NetworkR24AG044396 · NIA · MAYO CLINIC ROCHESTER · PI KIRKLAND, JAMES L. · 2013 to 2015
$684k
Removal of Senescent Cells for Adipose-derived Stem Cell TransplantsF30AG046061 · NIA · MAYO CLINIC ROCHESTER · PI PALMER, ALLYSON K · 2013 to 2017
$204k
NIA NIH HHS AG013925NIA NIH HHS AG044396NIA NIH HHS F30 AG046061NIA NIH HHS F30AG046061NIA NIH HHS P01 AG041122NIA NIH HHS R01 AG013925NIA NIH HHS R01 AG026094NIA NIH HHS R24 AG044396
6 · The paper itself

Abstract

Cellular senescence is a fundamental aging mechanism that has been implicated in many age-related diseases and is a significant cause of tissue dysfunction. Accumulation of senescent cells occurs during aging and is also seen in the context of obesity and diabetes. Senescent cells may play a role in type 2 diabetes pathogenesis through direct impact on pancreatic β-cell function, senescence-associated secretory phenotype (SASP)-mediated tissue damage, and involvement in adipose tissue dysfunction. In turn, metabolic and signaling changes seen in diabetes, such as high circulating glucose, altered lipid metabolism, and growth hormone axis perturbations, can promote senescent cell formation. Thus, senescent cells might be part of a pathogenic loop in diabetes, as both a cause and consequence of metabolic changes and tissue damage. Therapeutic targeting of a basic aging mechanism such as cellular senescence may have a large impact on disease pathogenesis and could be more effective in preventing the progression of diabetes complications than currently available therapies that have limited impact on already existing tissue damage. Therefore, senescent cells and the SASP represent significant opportunities for advancement in the prevention and treatment of type 2 diabetes and its complications.

Indexed as

Cellular SenescenceAdipose TissueAnimalsCellular MicroenvironmentCeramidesDiabetes Mellitus, Type 2HumansInsulin-Like Growth Factor Binding Protein 3Insulin-Like Growth Factor IInsulin ResistanceInsulin-Secreting CellsCeramidesIGFBP3 protein, humanInsulin-Like Growth Factor Binding Protein 3Insulin-Like Growth Factor I

Identifiers

PMID26106186
PMCPMC4477358
OpenAlexW1908141864

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.