Evidence map›Paper›PMID 22699503›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2012

Hypoxia-inducible factor 1 transcriptional activity in endothelial cells is required for acute phase cardioprotection induced by ischemic preconditioning.

Kakali Sarkar, Zheqing Cai, Rigu Gupta, Nirmal Parajuli, Karen Fox-Talbot, Medha S Darshan, Frank J Gonzalez, Gregg L Semenza

Open access · bronzeAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 62 papers.

0numbers the graph read from it
0cells of the map it votes in
62citing papers in PubMed
3.3field-weighted citation impact, top 8% 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, 96 citations in OpenAlex.

  1. Trial
  2. Review
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  4. Article
  5. Unraveling the Roles of HIF-1, HO-1, GLUT-1 and GLUT-4 in Myocardial Protection.International journal of drug discovery and pharmacology · 2024
    Article
  6. Article
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  9. Effect of vitamin B12 on methotrexate-induced cardiotoxicity in rats.Iranian journal of basic medical sciences · 2024
    Article
  10. Review
  11. Review
  12. Review
  13. Article
  14. Article
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  17. Article
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  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

8 authors at 3 institutions in 1 country.

Kakali SarkarVascular Program, Institute for Cell Engineering and Departments of Medicine, and McKusick-Nathans Institute of Genetic Medicine, The Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA.
Zheqing Cai
Rigu Gupta
Nirmal Parajuli
Karen Fox-Talbot
Medha S Darshan
Frank J Gonzalez
Gregg L Semenza
Johns Hopkins Medicine · USNational Institutes of Health · USRadiation Oncology Associates · US

Funding

Stat3 in Post-Ischemic Myocardial InflammationP01HL065608 · NHLBI · JOHNS HOPKINS UNIVERSITY · PI BECKER, LEWIS C · 2000 to 2011
$22.0M
NHLBI NIH HHS P01 HL065608NHLBI NIH HHS P01-HL65608
6 · The paper itself

Abstract

Infarction occurs when myocardial perfusion is interrupted for prolonged periods of time. Short episodes of ischemia and reperfusion protect against tissue injury when the heart is subjected to a subsequent prolonged ischemic episode, a phenomenon known as ischemic preconditioning (IPC). Hypoxia-inducible factor 1 (HIF-1) is a transcription factor that mediates adaptive responses to hypoxia/ischemia and is required for IPC. In this study, we performed a cellular and molecular characterization of the role of HIF-1 in IPC. We analyzed mice with knockout of HIF-1α or HIF-1β in Tie2(+) lineage cells, which include bone marrow (BM) and vascular endothelial cells, compared with control littermates. Hearts were subjected to 30 min of ischemia and 120 min of reperfusion, either as ex vivo Langendorff preparations or by in situ occlusion of the left anterior descending artery. The IPC stimulus consisted of two cycles of 5-min ischemia and 5-min reperfusion. Mice lacking HIF-1α or HIF-1β in Tie2(+) lineage cells showed complete absence of protection induced by IPC, whereas significant protection was induced by adenosine infusion. Treatment of mice with a HIF-1 inhibitor (digoxin or acriflavine) 4 h before Langendorff perfusion resulted in loss of IPC, as did administration of acriflavine directly into the perfusate immediately before IPC. We conclude that HIF-1 activity in endothelial cells is required for acute IPC. Expression and dimerization of the HIF-1α and HIF-1β subunits is required, suggesting that the heterodimer is functioning as a transcriptional activator, despite the acute nature of the response.

Indexed as

Ischemic PreconditioningTranscription, GeneticAnimalsBase SequenceCell LineageDNA PrimersHypoxia-Inducible Factor 1MiceMice, KnockoutDNA PrimersHypoxia-Inducible Factor 1

Identifiers

PMID22699503
PMCPMC3387090
OpenAlexW2103645671

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.