Evidence map›Paper›PMID 11238910›Full record

ArticleMolecular and cellular biology2001

Cardiomyopathy in Irx4-deficient mice is preceded by abnormal ventricular gene expression.

B G Bruneau, Z Z Bao, D Fatkin, J Xavier-Neto, D Georgakopoulos, C T Maguire, C I Berul, D A Kass, M L Kuroski-de Bold, A J de Bold and 5 more

Open access · greenAbstract read
In one paragraph

Article in Molecular and cellular biology, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 65 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
65citing papers in PubMed, 1 pooled it
4.1field-weighted citation impact, top 5% 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

65 citing papers in PubMed, 1 synthesis or guideline pooled it, 164 citations in OpenAlex.

  1. Pooled it
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  4. Review
  5. Article
  6. SHP2 genetic variants in NSML-associated RASopathies disrupt the PZR-IRX transcription factor signaling axis.Proceedings of the National Academy of Sciences of the United States of America · 2025
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5 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

15 authors at 6 institutions in 3 countries.

B G BruneauDepartment of Genetics, Harvard Medical School, Boston, Massachusetts 02115, USA.
Z Z Bao
D Fatkin
J Xavier-Neto
D Georgakopoulos
C T Maguire
C I Berul
D A Kass
M L Kuroski-de Bold
A J de Bold
D A Conner
N Rosenthal
C L Cepko
C E Seidman
J G Seidman
Harvard University Press · USHoward Hughes Medical Institute · USBrigham and Women's Hospital · USJohns Hopkins University · USOttawa Hospital · CAHarvard University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

To define the role of Irx4, a member of the Iroquois family of homeobox transcription factors in mammalian heart development and function, we disrupted the murine Irx4 gene. Cardiac morphology in Irx4-deficient mice (designated Irx4(Delta ex2/Delta ex2)) was normal during embryogenesis and in early postnatal life. Adult Irx4(Delta ex2/Delta ex2) mice developed a cardiomyopathy characterized by cardiac hypertrophy and impaired contractile function. Prior to the development of cardiomyopathy, Irx4(Delta ex2/Delta ex2) hearts had abnormal ventricular gene expression: Irx4-deficient embryos exhibited reduced ventricular expression of the basic helix-loop-helix transcription factor eHand (Hand1), increased Irx2 expression, and ventricular induction of an atrial chamber-specific transgene. In neonatal hearts, ventricular expression of atrial natriuretic factor and alpha-skeletal actin was markedly increased. Several weeks subsequent to these changes in embryonic and neonatal gene expression, increased expression of hypertrophic markers BNP and beta-myosin heavy chain accompanied adult-onset cardiac hypertrophy. Cardiac expression of Irx1, Irx2, and Irx5 may partially compensate for loss of Irx4 function. We conclude that Irx4 is not sufficient for ventricular chamber formation but is required for the establishment of some components of a ventricle-specific gene expression program. In the absence of genes under the control of Irx4, ventricular function deteriorates and cardiomyopathy ensues.

Indexed as

Gene Expression Regulation, DevelopmentalActinsAllelesAnimalsAtrial Natriuretic FactorBasic Helix-Loop-Helix ProteinsBlotting, NorthernCardiomyopathiesCytokinesDNA-Binding ProteinsDNA, ComplementaryDown-RegulationEchocardiographyHeterozygoteHomeodomain ProteinsHomozygoteActinsAtrial Natriuretic FactorBasic Helix-Loop-Helix ProteinsCytokinesDNA-Binding ProteinsDNA, ComplementaryHand1 protein, mousehelix-loop-helix protein, eHANDHomeodomain ProteinsIrx1 protein, mouseIRX 2Irx2 protein, mouseIrx4 protein, mouseIrx5 protein, mouseTranscription Factors

Identifiers

PMID11238910
PMCPMC86719
OpenAlexW2112567404

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.