Evidence map›Paper›PMID 21493702›Full record

ArticleCardiovascular research2011

IQGAP1 regulates ERK1/2 and AKT signalling in the heart and sustains functional remodelling upon pressure overload.

Mauro Sbroggiò, Daniela Carnevale, Alessandro Bertero, Giuseppe Cifelli, Emanuele De Blasio, Giada Mascio, Emilio Hirsch, Wadie F Bahou, Emilia Turco, Lorenzo Silengo and 3 more

Open access · bronzeAbstract read
In one paragraph

Article in Cardiovascular research, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers.

0numbers the graph read from it
0cells of the map it votes in
57citing papers in PubMed
3.5field-weighted citation impact, top 7% 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

57 citing papers in PubMed, 98 citations in OpenAlex.

  1. Queue Gaps Among the IQGAPs inInternational journal of molecular sciences · 2026
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  14. TANK Promotes Pressure Overload Induced Cardiac HypertrophyFrontiers in cardiovascular medicine · 2021
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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

13 authors at 3 institutions in 2 countries.

Mauro SbroggiòDipartimento di Genetica, Biologia e Biochimica, Molecular Biotechnology Center, Università di Torino, via Nizza 52, Turin, Italy.
Daniela Carnevale
Alessandro Bertero
Giuseppe Cifelli
Emanuele De Blasio
Giada Mascio
Emilio Hirsch
Wadie F Bahou
Emilia Turco
Lorenzo Silengo
Mara Brancaccio
Giuseppe Lembo
Guido Tarone
University of Turin · ITIstituto Neurologico Mediterraneo · ITStony Brook University · US

Funding

Platelet Systems Biology in Health and DiseaseR01HL119096 · NHLBI · STATE UNIVERSITY NEW YORK STONY BROOK · PI BAHOU, WADIE F · 2015 to 2019
$3.5M
Genetic dissection of the platelet thrombohemorrhagic phenotypeR01HL091939 · NHLBI · STATE UNIVERSITY NEW YORK STONY BROOK · PI BAHOU, WADIE F · 2009 to 2012
$1.6M
NHLBI NIH HHS R01 HL091939NHLBI NIH HHS R01 HL119096
6 · The paper itself

Abstract

aimsThe Raf-MEK1/2-ERK1/2 (ERK1/2-extracellular signal-regulated kinases 1/2) signalling cascade is crucial in triggering cardiac responses to different stress stimuli. Scaffold proteins are key elements in coordinating signalling molecules for their appropriate spatiotemporal activation. Here, we investigated the role of IQ motif-containing GTPase-activating protein 1 (IQGAP1), a scaffold for the ERK1/2 cascade, in heart function and remodelling in response to pressure overload. METHODS AND

resultsIQGAP1-null mice have unaltered basal heart function. When subjected to pressure overload, IQGAP1-null mice initially develop a compensatory hypertrophy indistinguishable from that of wild-type (WT) mice. However, upon a prolonged stimulus, the hypertrophic response develops towards a thinning of left ventricular walls, chamber dilation, and a decrease in contractility, in an accelerated fashion compared with WT mice. This unfavourable cardiac remodelling is characterized by blunted reactivation of the foetal gene programme, impaired cardiomyocyte hypertrophy, and increased cardiomyocyte apoptosis. Analysis of signalling pathways revealed two temporally distinct waves of both ERK1/2 and AKT phosphorylation peaking, respectively, at 10 min and 4 days after aortic banding in WT hearts. IQGAP1-null mice show strongly impaired phosphorylation of MEK1/2-ERK1/2 and AKT following 4 days of pressure overload, but normal activation of these kinases after 10 min. Pull-down experiments indicated that IQGAP1 is able to bind the three components of the ERK cascade, namely c-Raf, MEK1/2, and ERK1/2, as well as AKT in the heart.

conclusionThese data demonstrate, for the first time, a key role for the scaffold protein IQGAP1 in integrating hypertrophy and survival signals in the heart and regulating long-term left ventricle remodelling upon pressure overload.

Indexed as

Blood PressureSignal TransductionVentricular RemodelingAnimalsAortaApoptosisCells, CulturedDisease Models, AnimalHypertensionHypertrophy, Left VentricularLigationMaleMAP Kinase Kinase 1MAP Kinase Kinase 2MiceMice, 129 StrainIQ motif containing GTPase activating protein 1Map2k1 protein, mouseMap2k2 protein, mouseMapk1 protein, mouseMAP Kinase Kinase 1MAP Kinase Kinase 2Mitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3Proto-Oncogene Proteins c-aktProto-Oncogene Proteins c-rafras GTPase-Activating Proteins

Identifiers

PMID21493702
PMCPMC3294280
OpenAlexW2140239096

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.