Evidence map›Paper›PMID 30590424›Full record

ArticleThe journals of gerontology. Series A, Biological sciences and medical sciences2019

Adipose Tissue Senescence and Inflammation in Aging is Reversed by the Young Milieu.

Amiya Kumar Ghosh, Martin O'Brien, Theresa Mau, Nathan Qi, Raymond Yung

Open access · bronzeAbstract read
In one paragraph

Article in The journals of gerontology. Series A, Biological sciences and medical sciences, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.

0numbers the graph read from it
0cells of the map it votes in
44citing papers in PubMed
2.9field-weighted citation impact, top 9% 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

44 citing papers in PubMed, 70 citations in OpenAlex.

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  14. mAging and disease · 2024
    Article
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  19. Adipocyte Microenvironment in Ovarian Cancer: A Critical Contributor?International journal of molecular sciences · 2023
    Review
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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

5 authors at 1 institution in 1 country.

Amiya Kumar GhoshDivision of Geriatric and Palliative Medicine, University of Michigan, Ann Arbor.
Martin O'BrienDivision of Geriatric and Palliative Medicine, University of Michigan, Ann Arbor.
Theresa MauDivision of Geriatric and Palliative Medicine, University of Michigan, Ann Arbor.
Nathan QiAnimal Phenotyping Core, Division of Metabolism, Endocrinology, and Diabetes, Department of Internal Medicine, University of Michigan, Ann Arbor.
Raymond YungDivision of Geriatric and Palliative Medicine, University of Michigan, Ann Arbor.
University of Michigan–Ann Arbor · US

Funding

Research Education CoreP30AG024824 · NIA · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI Neil Alexander · 2004 to 2026
$29.2M
Research Training in BiogerontologyT32AG000114 · NIA · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI SCOTT PLETCHER · 1985 to 2026
$12.4M
RESEARCH TRAINING IN EXPERIMENTAL IMMUNOPATHOLOGYT32AI007413 · NIAID · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI Bethany B. Moore · 1993 to 2026
$9.8M
Michigan Mouse Metabolic Phenotyping CenterU2CDK110768 · NIDDK · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI ELIAS, CAROL FUZETI · 2016 to 2021
$6.2M
NIAID NIH HHS T32 AI007413NIA NIH HHS P30 AG024824NIA NIH HHS T32 AG000114NIDDK NIH HHS U2C DK110768
6 · The paper itself

Abstract

Visceral adipose tissue (VAT) inflammation plays a central role in longevity and multiple age-related disorders. Cellular senescence (SEN) is a fundamental aging mechanism that contributes to age-related chronic inflammation and organ dysfunction, including VAT. Recent studies using heterochronic parabiosis models strongly suggested that circulating factors in young plasma alter the aging phenotypes of old animals. Our study investigated if young plasma rescued SEN phenotypes in the VAT of aging mice. With heterochronic parabiosis model using young (3 months) and old (18 months) mice, we found significant reduction in the levels of pro-inflammatory cytokines and altered adipokine profile that are protective of SEN in the VAT of old mice. These data are indicative of protection from SEN of aging VAT by young blood circulation. Old parabionts also exhibited diminished expression of cyclin-dependent kinase inhibitors (CDKi) genes p16 (Cdkn2a) and p21 (Cdkn1a/Cip1) in the VAT. In addition, when exposed to young serum condition in an ex vivo culture system, aging adipose tissue-derived stromovascular fraction cells produced significantly lower amounts of pro-inflammatory cytokines (MCP-1 and IL-6) compared to old condition. Expressions of p16 and p21 genes were also diminished in the old stromovascular fraction cells under young serum condition. Finally, in 3T3-preadipocytes culture system, we found reduced pro-inflammatory cytokines (Mcp-1 and Il-6) and diminished expression of cyclin-dependent kinase inhibitor genes in the presence of young serum compared to old serum. In summary, this study demonstrates that young milieu is capable of protecting aging adipose tissue from SEN and thereby inflammation.

Indexed as

Age FactorsAgingAnalysis of VarianceAnimalsCells, CulturedCellular SenescenceChemokine CCL2Cyclin-Dependent Kinase Inhibitor ProteinsCytokinesDisease Models, AnimalInflammationInterleukin-6Intra-Abdominal FatMaleMice, Inbred C57BLParabiosisCcl2 protein, mouseChemokine CCL2Cyclin-Dependent Kinase Inhibitor ProteinsCytokinesInterleukin-6Adipose tissueAgingInflammationPlasma factorsSenescence

Identifiers

PMID30590424
PMCPMC6777079
OpenAlexW2905809405

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.