Evidence map›Paper›PMID 9207128›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America1997

Angiotensin II type1a receptor gene expression in the heart: AP-1 and GATA-4 participate in the response to pressure overload.

T C Herzig, S M Jobe, H Aoki, J D Molkentin, A W Cowley, S Izumo, B E Markham

Open access · greenAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 1997. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.

0numbers the graph read from it
0cells of the map it votes in
47citing papers in PubMed
5.6field-weighted citation impact, top 3% 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

47 citing papers in PubMed, 197 citations in OpenAlex.

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  10. Myocardial plasticity: cardiac development, regeneration and disease.Current opinion in genetics & development · 2016
    Review
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  16. Modulation of angiotensin II signaling following exercise training in heart failure.American journal of physiology. Heart and circulatory physiology · 2015
    Review
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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 2 institutions in 1 country.

T C HerzigDepartment of Physiology, Medical College of Wisconsin, 8701 Watertown Plank Road, Milwaukee, WI 53226, USA.
S M Jobe
H Aoki
J D Molkentin
A W Cowley
S Izumo
B E Markham
Medical College of Wisconsin · USUniversity of Michigan–Ann Arbor · US

Funding

VASOPRESSIN SECRETION AND CARDIOVASCULAR FUNCTIONP01HL029587 · NHLBI · MEDICAL COLLEGE OF WISCONSIN · PI COWLEY, ALLEN W · 1985 to 2012
$24.1M
INTRACELLULAR PATHWAYS THAT MEDIATE CARDIAC HYPERTROPHYR01HL043662 · NHLBI · PARKE DAVIS PHARMACEUTICAL RESEARCH DIV · PI MARKHAM, BRUCE E. · 1990 to 1997
–
NHLBI NIH HHS HL29587NHLBI NIH HHS HL43662NHLBI NIH HHS P01 HL029587
6 · The paper itself

Abstract

Hypertrophy of mammalian cardiac muscle is mediated, in part, by angiotensin II through an angiotensin II type1a receptor (AT1aR)-dependent mechanism. To understand how the level of AT1aRs is altered in this pathological state, we studied the expression of an injected AT1aR promoter-luciferase reporter gene in adult rat hearts subjected to an acute pressure overload by aortic coarctation. This model was validated by demonstrating that coarctation increased expression of the alpha-skeletal actin promoter 1.7-fold whereas the alpha-myosin heavy chain promoter was unaffected. Pressure overload increased expression from the AT1aR promoter by 1. 6-fold compared with controls. Mutations introduced into consensus binding sites for AP-1 or GATA transcription factors abolished the pressure overload response but had no effect on AT1aR promoter activity in control animals. In extracts from coarcted hearts, but not from control hearts, a Fos-JunB-JunD complex and GATA-4 were detected in association with the AP-1 and GATA sites, respectively. These results establish that the AT1aR promoter is active in cardiac muscle and its expression is induced by pressure overload, and suggest that this response is mediated, in part, by a functional interaction between AP-1 and GATA-4 transcription factors.

Indexed as

Gene Expression RegulationAnimalsAortic CoarctationBinding SitesBlood PressureCells, CulturedDNA-Binding ProteinsErythroid-Specific DNA-Binding FactorsGene Transfer TechniquesHeartMaleMutationMyocardiumRatsRats, Sprague-DawleyRats, WistarDNA-Binding ProteinsErythroid-Specific DNA-Binding FactorsReceptors, AngiotensinTranscription Factor AP-1Transcription Factors

Identifiers

PMID9207128
PMCPMC23858
OpenAlexW2047866697

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.