Evidence map›Paper›PMID 21169469›Full record

ArticleAmerican journal of respiratory and critical care medicine2011

Yin yang 1 is a novel regulator of pulmonary fibrosis.

Xin Lin, Patricia J Sime, Haodong Xu, Marc A Williams, Larry LaRussa, Steve N Georas, Jia Guo

Abstract read
In one paragraph

Article in American journal of respiratory and critical care medicine, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
2.4field-weighted citation impact, top 11% 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

31 citing papers in PubMed, 59 citations in OpenAlex.

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  11. Innate Immune Responses and Pulmonary Diseases.Advances in experimental medicine and biology · 2021
    Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Myofibroblast-specific YY1 promotes liver fibrosis.Biochemical and biophysical research communications · 2019
    Article
  17. Article
  18. Exosome-Mediated miR-29 Transfer Reduces Muscle Atrophy and Kidney Fibrosis in Mice.Molecular therapy : the journal of the American Society of Gene Therapy · 2019
    Article
  19. Review
  20. Article
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

7 authors at 1 institution in 1 country.

Xin LinDepartment of Medicine, University of Rochester Medical School, Rochester, New York 14642, USA.
Patricia J Sime
Haodong Xu
Marc A Williams
Larry LaRussa
Steve N Georas
Jia Guo
University of Rochester Medical Center · US

Funding

Modulation of Silica-Induced Pulmonary FibrosisR01HL075432 · NHLBI · UNIVERSITY OF ROCHESTER · PI SIME, PATRICIA JANET · 2005 to 2009
$2.0M
Yin-Yang-1:a novel transcription factor in Th responsesR01HL073952 · NHLBI · UNIVERSITY OF ROCHESTER · PI GEORAS, STEVE NICHOLAS · 2003 to 2006
$1.6M
Pathways to FibrosisR03HL095402 · NHLBI · UNIVERSITY OF ROCHESTER · PI PHIPPS, RICHARD P., SIME, PATRICIA JANET · 2008 to 2009
$154k
CSR NIH HHS RG-10327-NNHLBI NIH HHS HL095402NHLBI NIH HHS HL75432NHLBI NIH HHS R01 HL073952
6 · The paper itself

Abstract

rationaleThe differentiation of fibroblasts into myofibroblasts is a cardinal feature of idiopathic pulmonary fibrosis (IPF). The transcription factor Yin Yang 1 (YY1) plays a role in the proliferation and differentiation of diverse cell types, but its role in fibrotic lung diseases is not known.

objectivesTo elucidate the mechanism by which YY1 regulates fibroblast differentiation and lung fibrosis.

methodsLung fibroblasts were cultured with transforming growth factor (TGF)-β or tumor necrosis factor-α. Nuclear factor (NF)-κB, YY1, and α-smooth muscle actin (SMA) were determined in protein, mRNA, and promoter reporter level. Lung fibroblasts and lung fibrosis were assessed in a partial YY1-deficient mouse and a YY1(f/f) conditional knockout mouse after being exposed to silica or bleomycin. MEASUREMENTS AND MAIN

resultsTGF-β and tumor necrosis factor-α up-regulated YY1 expression in lung fibroblasts. TGF-β-induced YY1 expression was dramatically decreased by an inhibitor of NF-κB, which blocked I-κB degradation. YY1 is significantly overexpressed in both human IPF and murine models of lung fibrosis, including in the aggregated pulmonary fibroblasts of fibrotic foci. Furthermore, the mechanism of fibrogenesis is that YY1 can up-regulate α-SMA expression in pulmonary fibroblasts. YY1-deficient (YY1(+/-)) mice were significantly protected from lung fibrosis, which was associated with attenuated α-SMA and collagen expression. Finally, decreasing YY1 expression through instilled adenovirus-cre in floxed-YY1(f/f) mice reduced lung fibrosis.

conclusionsYY1 is overexpressed in fibroblasts in both human IPF and murine models in a NF-κB-dependent manner, and YY1 regulates fibrogenesis at least in part by increasing α-SMA and collagen expression. Decreasing YY1 expression may provide a new therapeutic strategy for pulmonary fibrosis.

Indexed as

ActinsAnimalsCell DifferentiationCell ProliferationCells, CulturedFibroblastsFluorescent Antibody TechniqueHumansLungMiceNF-kappa BPulmonary FibrosisTransforming Growth Factor betaTumor Necrosis Factor-alphaUp-RegulationYY1 Transcription FactorACTA2 protein, humanActinsNF-kappa BTransforming Growth Factor betaTumor Necrosis Factor-alphaYY1 Transcription Factor

Identifiers

PMID21169469
PMCPMC3136995
OpenAlexW2101900404

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.