Evidence map›Paper›PMID 26678048›Full record

ArticlePLoS genetics2015

The Inflammatory Transcription Factors NFκB, STAT1 and STAT3 Drive Age-Associated Transcriptional Changes in the Human Kidney.

Zach K O'Brown, Eric L Van Nostrand, John P Higgins, Stuart K Kim

Open access · goldAbstract read
In one paragraph

Article in PLoS genetics, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 62 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
62citing papers in PubMed, 1 pooled it
4.3field-weighted citation impact, top 6% 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

62 citing papers in PubMed, 1 synthesis or guideline pooled it, 89 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Multi-Omics Data Reveal Estrogen-Driven Dysregulation and Stromal-Epithelial Signaling Alterations in Endometrial Polyps.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026
    Article
  5. Article
  6. Review
  7. Article
  8. Review
  9. Article
  10. Article
  11. Review
  12. Gene regulatory networks in disease and ageing.Nature reviews. Nephrology · 2024
    Review
  13. Article
  14. Article
  15. Article
  16. Cellular senescence and kidney aging.Clinical science (London, England : 1979) · 2023
    Review
  17. Article
  18. Article
  19. Article
  20. Article

2 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 3 institutions in 1 country.

Zach K O'BrownDepartment of Developmental Biology, Stanford University, Stanford, California, United States of America.
Eric L Van NostrandDepartment of Cellular and Molecular Medicine, University of California, San Diego, La Jolla, California, United States of America.
John P HigginsDepartment of Pathology, Stanford University Medical Center, Stanford, California, United States of America.
Stuart K KimDepartment of Developmental Biology, Stanford University, Stanford, California, United States of America.
Stanford University · USStanford Medicine · USUniversity of California, San Diego · US

Funding

Leveraging innovative technologies in basic and clinical cancer researchT32CA009302 · NCI · STANFORD UNIVERSITY · PI LAURA D ATTARDI, Aaron M Newman · 1985 to 2026
$19.1M
Mechanisms of Aging in C. elegansR01AG025941 · NIA · STANFORD UNIVERSITY · PI DAVIS, RONALD WAYNE · 2007 to 2017
$3.1M
NCI NIH HHS CA09302NCI NIH HHS T32 CA009302NIA NIH HHS R01 AG0250941NIA NIH HHS R01 AG025941
6 · The paper itself

Abstract

Human kidney function declines with age, accompanied by stereotyped changes in gene expression and histopathology, but the mechanisms underlying these changes are largely unknown. To identify potential regulators of kidney aging, we compared age-associated transcriptional changes in the human kidney with genome-wide maps of transcription factor occupancy from ChIP-seq datasets in human cells. The strongest candidates were the inflammation-associated transcription factors NFκB, STAT1 and STAT3, the activities of which increase with age in epithelial compartments of the renal cortex. Stimulation of renal tubular epithelial cells with the inflammatory cytokines IL-6 (a STAT3 activator), IFNγ (a STAT1 activator), or TNFα (an NFκB activator) recapitulated age-associated gene expression changes. We show that common DNA variants in RELA and NFKB1, the two genes encoding subunits of the NFκB transcription factor, associate with kidney function and chronic kidney disease in gene association studies, providing the first evidence that genetic variation in NFκB contributes to renal aging phenotypes. Our results suggest that NFκB, STAT1 and STAT3 underlie transcriptional changes and chronic inflammation in the aging human kidney.

Indexed as

AgingGenetic Association StudiesHumansInflammationInterferon-gammaInterleukin-6NF-kappa BNF-kappa B p50 SubunitRenal Insufficiency, ChronicSTAT1 Transcription FactorSTAT3 Transcription FactorTranscription Factor RelATranscription, GeneticTumor Necrosis Factor-alphaIL6 protein, humanInterferon-gammaInterleukin-6NF-kappa BNF-kappa B p50 SubunitNFKB1 protein, humanRELA protein, humanSTAT1 protein, humanSTAT1 Transcription FactorSTAT3 protein, humanSTAT3 Transcription FactorTranscription Factor RelATumor Necrosis Factor-alpha

Identifiers

PMID26678048
PMCPMC4682820
OpenAlexW2215361131

What OpenQuestion holds

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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.