Evidence map›Paper›PMID 20701600›Full record

ReviewAging cell2010

Fat tissue, aging, and cellular senescence.

Tamara Tchkonia, Dean E Morbeck, Thomas Von Zglinicki, Jan Van Deursen, Joseph Lustgarten, Heidi Scrable, Sundeep Khosla, Michael D Jensen, James L Kirkland

Open access · bronzeAbstract readReview
In one paragraph

Review in Aging cell, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 631 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
631citing papers in PubMed, 1 pooled it
15.8field-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

631 citing papers in PubMed, 1 synthesis or guideline pooled it, 1,074 citations in OpenAlex.

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571 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

9 authors at 1 institution in 1 country.

Tamara TchkoniaRobert and Arlene Kogod Center on Aging, Mayo Clinic, Rochester, MN 55905, USA.
Dean E Morbeck
Thomas Von Zglinicki
Jan Van Deursen
Joseph Lustgarten
Heidi Scrable
Sundeep Khosla
Michael D Jensen
James L Kirkland
Mayo Clinic in Florida · US

Funding

REGIONAL FATTY ACID METABOLISM IN HUMANSR01DK045343 · NIDDK · MAYO CLINIC ROCHESTER · PI MICHAEL D. JENSEN · 1992 to 2026
$12.9M
The Somatotropic Axis and Health Aging: A Search for MechanismsP01AG031736 · NIA · SOUTHERN ILLINOIS UNIVERSITY SCH OF MED · PI KIRKLAND, JAMES L. · 2009 to 2013
$8.4M
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
Mechanism of Action of CpG-ODN in Generating Tumor Immunity in the AgedR01AG028751 · NIA · MAYO CLINIC ARIZONA · PI GENDLER, SANDRA J · 2007 to 2011
$1.6M
Medical Research Council G0601333Medical Research Council G0900686NIA NIH HHS AG13925NIA NIH HHS AG31736NIA NIH HHS P01 AG031736NIA NIH HHS R01 AG013925NIA NIH HHS R01 AG028751NIA NIH HHS R37 AG013925NIDDK NIH HHS R01 DK045343
6 · The paper itself

Abstract

Fat tissue, frequently the largest organ in humans, is at the nexus of mechanisms involved in longevity and age-related metabolic dysfunction. Fat distribution and function change dramatically throughout life. Obesity is associated with accelerated onset of diseases common in old age, while fat ablation and certain mutations affecting fat increase life span. Fat cells turn over throughout the life span. Fat cell progenitors, preadipocytes, are abundant, closely related to macrophages, and dysdifferentiate in old age, switching into a pro-inflammatory, tissue-remodeling, senescent-like state. Other mesenchymal progenitors also can acquire a pro-inflammatory, adipocyte-like phenotype with aging. We propose a hypothetical model in which cellular stress and preadipocyte overutilization with aging induce cellular senescence, leading to impaired adipogenesis, failure to sequester lipotoxic fatty acids, inflammatory cytokine and chemokine generation, and innate and adaptive immune response activation. These pro-inflammatory processes may amplify each other and have systemic consequences. This model is consistent with recent concepts about cellular senescence as a stress-responsive, adaptive phenotype that develops through multiple stages, including major metabolic and secretory readjustments, which can spread from cell to cell and can occur at any point during life. Senescence could be an alternative cell fate that develops in response to injury or metabolic dysfunction and might occur in nondividing as well as dividing cells. Consistent with this, a senescent-like state can develop in preadipocytes and fat cells from young obese individuals. Senescent, pro-inflammatory cells in fat could have profound clinical consequences because of the large size of the fat organ and its central metabolic role.

Indexed as

Adipose TissueAgingCellular SenescenceAnimalsHumans

Identifiers

PMID20701600
PMCPMC2941545
OpenAlexW2131250713

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.