Evidence map›Paper›PMID 19696070›Full record

ArticleCardiovascular research2010

Role of nuclear unphosphorylated STAT3 in angiotensin II type 1 receptor-induced cardiac hypertrophy.

Hong Yue, Wei Li, Russell Desnoyer, Sadashiva S Karnik

Open access · bronzeAbstract read
In one paragraph

Article in Cardiovascular research, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
46citing papers in PubMed, 1 pooled it
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

46 citing papers in PubMed, 1 synthesis or guideline pooled it, 84 citations in OpenAlex.

  1. Pooled it
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  4. The regulatory roles of STAT3 protein in the pathogenesis of viral infections.Frontiers in cellular and infection microbiology · 2025
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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

4 authors at 2 institutions in 1 country.

Hong YueDepartment of Molecular Cardiology, Lerner Research Institute, Cleveland Clinic, Cleveland, OH 44195, USA.
Wei Li
Russell Desnoyer
Sadashiva S Karnik
Cleveland Clinic · USCleveland Clinic Lerner College of Medicine · US

Funding

Molecular Basis of Ang II Receptor FunctionsR01HL057470 · NHLBI · CLEVELAND CLINIC LERNER COM-CWRU · PI KARNIK, SADASHIVA S · 1997 to 2013
$4.4M
Phosphoproteome and Ang II-induced VSMC Gene ExpressionR01HL083243 · NHLBI · CLEVELAND CLINIC LERNER COM-CWRU · PI KARNIK, SADASHIVA S · 2006 to 2010
$1.6M
Regulation of AT1R-signaling and pathology in vessels through microRNAR01HL115964 · NHLBI · CLEVELAND CLINIC LERNER COM-CWRU · PI KARNIK, SADASHIVA S · 2012 to 2015
$1.5M
NHLBI NIH HHS HL083243NHLBI NIH HHS R01 HL057470NHLBI NIH HHS R01 HL083243NHLBI NIH HHS R01 HL115964NHLBI NIH HHS R01 HL57470
6 · The paper itself

Abstract

aimsCardiac hypertrophy is a risk factor independent of blood pressure; however, the mechanisms that distinguish pathological remodelling due to local cues from pressure overload are unresolved. This study was aimed at discovering a novel gene expression mechanism in heart failure. METHODS AND

resultsIn angiotensin II type 1 receptor (AT1R) transgenic mice (TG), we found a significant increase of mRNA and total STAT3 (T-STAT3) protein, but not STAT3 phosphorylated at residues Y705 and S727. A net increase in nuclear accumulation of this unphosphorylated form of STAT3 (U-STAT3) correlated with the development of cardiac hypertrophy and dysfunction, which are associated with abnormal expression of osteopontin and regulator of G protein signalling 2 genes. Nuclear accumulation of U-STAT3 is induced by angiotensin II treatment in neonatal cardiac myocytes, fibroblasts, and AT1R-expressing human embryonic kidney 293 (HEK-AT1R) cells. Chromatin immunoprecipitation demonstrated that U-STAT3 binds to the target gene promoter, and siRNA-mediated knockdown of STAT3 expression significantly altered the expression of target genes in HEK-AT1R cells. T-STAT3 in TG mouse hearts and the phosphorylation-deficient Y705F mutant STAT3 in HEK-AT1R cells physically interacted with transcription co-activator p300.

conclusionChronic activation of AT1R induces unregulated expression of the Stat3 gene, leading to nuclear accumulation of U-STAT3, which significantly correlated with progression of cardiac hypertrophy.

Indexed as

AnimalsCardiomegalyCell NucleusCells, CulturedGene Expression RegulationMiceMice, Inbred C57BLMyocytes, CardiacOsteoprotegerinp300-CBP Transcription FactorsPhosphorylationReceptor, Angiotensin, Type 1RGS ProteinsSTAT3 Transcription FactorOsteoprotegerinp300-CBP Transcription FactorsReceptor, Angiotensin, Type 1Rgs2 protein, mouseRGS ProteinsStat3 protein, mouseSTAT3 Transcription Factor

Identifiers

PMID19696070
PMCPMC2791056
OpenAlexW2022846817

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.