Evidence map›Paper›PMID 42769509›Full record

ArticleGeromedicine2026

The senescence-inhibitory p53 isoform Δ133p53α represses the proinflammatory chemokine CXCL10 in progeria model mice and naturally aged mice.

Leo Yamada, Huaitian Liu, Curtis C Harris, Izumi Horikawa

Abstract read
In one paragraph

Article in Geromedicine, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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0citing papers in PubMed
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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

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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

0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

4 authors.

Leo YamadaLaboratory of Human Carcinogenesis, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892, USA.ORCID 0000-0003-0179-4802
Huaitian LiuLaboratory of Human Carcinogenesis, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892, USA.ORCID 0000-0002-7791-1502
Curtis C HarrisLaboratory of Human Carcinogenesis, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892, USA.ORCID 0000-0001-5268-0181
Izumi HorikawaLaboratory of Human Carcinogenesis, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892, USA.ORCID 0000-0002-2893-5014

Funding

p53, Aging, and CancerZIABC011496 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI HARRIS, CURTIS · 2013 to 2025
$21.1M
Intramural NIH HHS ZIA BC011496
6 · The paper itself

Abstract

Aims: Δ133p53α is a naturally occurring isoform of the human p53 protein that inhibits p53-mediated cellular senescence. We previously reported that transgenic expression of this senescence-inhibitory p53 isoform counteracts aging-associated pathological changes in progeria model mice (heterozygous Methods: A Luminex-based multiplex quantitative assay was performed using mouse serum samples from transgenic Δ133p53α-expressing Results: In the Luminex assay, used as an exploratory screen, transgenic Δ133p53α expression was suggestively associated with reduced serum levels of not only IL-6 but also CXCL1, IL-1α, and CXCL10. We further characterized CXCL10, which has not previously been linked to progeria in mice or humans. Consistent with reduced serum CXCL10 levels, both young (15-week-old) and old (10-month-old) Δ133p53α-expressing Conclusion: CXCL10, a proinflammatory chemokine elevated in both accelerated and natural aging, is a potential target of the anti-inflammatory activity of Δ133p53α.

Indexed as

agingCXCL10human GTEx datasetLuminex assayp53 isoformprogeria miceproinflammatory chemokine

Identifiers

PMID42769509
PMCPMC13591461

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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.