Evidence map›Paper›PMID 24326162›Full record

ArticleJournal of the American Heart Association2013

Activation of hypoxia-inducible factor-2 in adipocytes results in pathological cardiac hypertrophy.

Qun Lin, Yan Huang, Carmen J Booth, Volker H Haase, Randall S Johnson, M Celeste Simon, Frank J Giordano, Zhong Yun

Open access · goldAbstract read
In one paragraph

Article in Journal of the American Heart Association, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
1.0field-weighted citation impact, top 22% 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

29 citing papers in PubMed, 51 citations in OpenAlex.

  1. Article
  2. Review
  3. Hypoxia signaling in the adipose tissue.Journal of molecular cell biology · 2025
    Review
  4. Article
  5. The Effect of HIF-2International journal of inflammation · 2025
    Review
  6. Article
  7. Article
  8. Review
  9. Review
  10. Review
  11. Updated perspective of EPAS1 and the role in pulmonary hypertension.Frontiers in cell and developmental biology · 2023
    Review
  12. Article
  13. Review
  14. Review
  15. Review
  16. Article
  17. Hypoxia signaling in human diseases and therapeutic targets.Experimental & molecular medicine · 2019
    Review
  18. Review
  19. Modulation of HIF-2α PAS-B domain contributes to physiological responses.Proceedings of the National Academy of Sciences of the United States of America · 2018
    Article
  20. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

8 authors at 4 institutions in 2 countries.

Qun LinDepartment of Therapeutic Radiology, Yale School of Medicine, New Haven, CT.
Yan Huang
Carmen J Booth
Volker H Haase
Randall S Johnson
M Celeste Simon
Frank J Giordano
Zhong Yun
Yale University · USUniversity of Cambridge · GBUniversity of Pennsylvania · USVanderbilt University · US

Funding

Transgenic CoreP30DK057521 · NIDDK · MASSACHUSETTS GENERAL HOSPITAL · PI FLOREZ, JOSE CARLOS · 2000 to 2019
$31.4M
Glucose Transporter Regulation in Obesity and DiabetesR37DK043051 · NIDDK · BETH ISRAEL DEACONESS MEDICAL CENTER · PI KAHN, BARBARA B. · 2006 to 2015
$5.0M
Molecular Mechanisms of Renal InjuryR01DK081646 · NIDDK · VANDERBILT UNIVERSITY MEDICAL CENTER · PI HAASE, VOLKER HANS · 2008 to 2021
$4.3M
Metabolic effects of adipose lipogenesisR01DK098002 · NIDDK · BETH ISRAEL DEACONESS MEDICAL CENTER · PI KAHN, BARBARA B., MCGRAW, TIMOTHY E · 2013 to 2016
$2.4M
Hypoxia-Inducible Factors in Liver MetabolismR01DK080821 · NIDDK · VANDERBILT UNIVERSITY · PI HAASE, VOLKER HANS · 2009 to 2013
$1.7M
Howard Hughes Medical InstituteNIDDK NIH HHS P30 DK57521NIDDK NIH HHS R01 DK080821NIDDK NIH HHS R01 DK081646NIDDK NIH HHS R01 DK098002NIDDK NIH HHS R37 DK43051Wellcome Trust 092738
6 · The paper itself

Abstract

backgroundObesity can cause structural and functional abnormalities of the heart via complex but largely undefined mechanisms. Emerging evidence has shown that obesity results in reduced oxygen concentrations, or hypoxia, in adipose tissue. We hypothesized that the adipocyte hypoxia-signaling pathway plays an essential role in the development of obesity-associated cardiomyopathy. METHODS AND

resultsUsing a mouse model in which the hypoxia-inducible factor (HIF) pathway is activated by deletion of the von Hippel-Lindau gene specifically in adipocytes, we found that mice with adipocyte-von Hippel-Lindau deletion developed lethal cardiac hypertrophy. HIF activation in adipocytes results in overexpression of key cardiomyopathy-associated genes in adipose tissue, increased serum levels of several proinflammatory cytokines including interleukin-1β and monocyte chemotactic protein-1, and activation of nuclear factor-κB and nuclear factor of activated T cells in the heart. Interestingly, genetic deletion of Hif2a, but not Hif1a, was able to rescue cardiac hypertrophy and abrogate adipose inflammation.

conclusionWe have discovered a previously uncharacterized mechanism underlying a critical and direct role of the adipocyte HIF-2 transcription factor in the development of adipose inflammation and pathological cardiac hypertrophy.

Indexed as

AdipocytesAnimalsBasic Helix-Loop-Helix ProteinsCardiomegalyCytokinesDisease Models, AnimalEndothelial PAS Domain-Containing Protein 1Gene Expression RegulationGenetic Predisposition to DiseaseHypoxia-Inducible Factor 1, alpha SubunitInflammation MediatorsMiceMice, Inbred C57BLMice, KnockoutMice, TransgenicMyocytes, CardiacBasic Helix-Loop-Helix ProteinsCytokinesEndothelial PAS Domain-Containing Protein 1Hif1a protein, mouseHypoxia-Inducible Factor 1, alpha SubunitInflammation MediatorsVHL protein, mouseVon Hippel-Lindau Tumor Suppressor Proteinadipocytescardiomyopathyhypoxiainflammationobesity

Identifiers

PMID24326162
PMCPMC3886757
OpenAlexW2167296832

What OpenQuestion holds

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LicenceCC BY-NC
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.