Evidence map›Paper›PMID 27866946›Full record

ArticleCell systems2017

Systems Genetics Approach Identifies Gene Pathways and Adamts2 as Drivers of Isoproterenol-Induced Cardiac Hypertrophy and Cardiomyopathy in Mice.

Christoph D Rau, Milagros C Romay, Mary Tuteryan, Jessica J-C Wang, Marc Santolini, Shuxun Ren, Alain Karma, James N Weiss, Yibin Wang, Aldons J Lusis

Open access · bronzeAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cell systems, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed
3.4field-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

38 citing papers in PubMed, 52 citations in OpenAlex.

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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

10 authors at 2 institutions in 1 country.

Christoph D RauDepartment of Microbiology, Immunology and Molecular Genetics, David Geffen School of Medicine, University of California, Los Angeles, Los Angeles, CA 90095, USA; Departments of Anesthesiology, Physiology, and Medicine, Cardiovascular Research Laboratories, David Geffen School of Medicine, University of California, Los Angeles, Los Angeles, CA 90095, USA.
Milagros C RomayDepartment of Microbiology, Immunology and Molecular Genetics, David Geffen School of Medicine, University of California, Los Angeles, Los Angeles, CA 90095, USA.
Mary TuteryanDepartment of Microbiology, Immunology and Molecular Genetics, David Geffen School of Medicine, University of California, Los Angeles, Los Angeles, CA 90095, USA.
Jessica J-C WangDepartment of Medicine, David Geffen School of Medicine, University of California, Los Angeles, Los Angeles, CA 90095, USA.
Marc SantoliniCenter for Interdisciplinary Research on Complex Systems, Department of Physics, Northeastern University, Boston, MA 02115, USA.
Shuxun RenDepartments of Anesthesiology, Physiology, and Medicine, Cardiovascular Research Laboratories, David Geffen School of Medicine, University of California, Los Angeles, Los Angeles, CA 90095, USA.
Alain KarmaCenter for Interdisciplinary Research on Complex Systems, Department of Physics, Northeastern University, Boston, MA 02115, USA.
James N WeissDepartment of Medicine, David Geffen School of Medicine, University of California, Los Angeles, Los Angeles, CA 90095, USA.
Yibin WangDepartments of Anesthesiology, Physiology, and Medicine, Cardiovascular Research Laboratories, David Geffen School of Medicine, University of California, Los Angeles, Los Angeles, CA 90095, USA.
Aldons J LusisDepartment of Microbiology, Immunology and Molecular Genetics, David Geffen School of Medicine, University of California, Los Angeles, Los Angeles, CA 90095, USA; Department of Medicine, David Geffen School of Medicine, University of California, Los Angeles, Los Angeles, CA 90095, USA; Department of Human Genetics, David Geffen School of Medicine, University of California, Los Angeles, Los Angeles, CA 90095, USA. Electronic address: jlusis@mednet.ucla.edu.
University of California, Los Angeles · USNortheastern University · US

Funding

Systems genomics of metabolic syndrome traitsP01HL028481 · NHLBI · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI LUSIS, ALDONS JAKE · 1985 to 2019
$50.2M
UCLA NIGMS T32 Program AssessmentT32GM007185 · NIGMS · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI TORRES, JORGE · 1985 to 2020
$21.7M
CARDIOVASCULAR SCIENTIST TRAINING PROGRAMT32HL007895 · NHLBI · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI SHIVKUMAR, KALYANAM, WATSON, KAROL E · 1998 to 2023
$9.2M
Vascular Biology Training GrantT32HL069766 · NHLBI · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI LUSIS, ALDONS JAKE · 2002 to 2022
$7.4M
Systems Approach to Unraveling the Genetic Basis of Heart FailureR01HL114437 · NHLBI · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI DENG, MARIO C., KARMA, ALAIN S · 2013 to 2016
$4.7M
Epigenomic Mechanisms of Heart FailureR01HL129639 · NHLBI · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI VONDRISKA, THOMAS M. · 2015 to 2018
$2.6M
A Systems Approach to Dissect Genetic Basis of Heart FailureR01HL123295 · NHLBI · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI LUSIS, ALDONS JAKE, WANG, YIBIN · 2014 to 2017
$2.6M
Novel Mechanisms of LncRNA Mediated Epigenetic Regulation in Cardiac HypertrophyR01HL143058 · NHLBI · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI VONDRISKA, THOMAS M. · 2018 to 2021
$2.2M
Functional Validation of Myh14 in Stress-Induced Cardiac Remodeling.K08HL133491 · NHLBI · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI WANG, JESSICA J · 2017 to 2021
$875k
A Systems Approach to Uncover Novel Genes and Networks in Heart FailureR21HL110667 · NHLBI · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI LUSIS, ALDONS JAKE, WANG, YIBIN · 2011 to 2012
$424k
NHLBI NIH HHS K08 HL133491NHLBI NIH HHS P01 HL028481NHLBI NIH HHS R01 HL114437NHLBI NIH HHS R01 HL123295NHLBI NIH HHS R01 HL129639NHLBI NIH HHS R01 HL143058NHLBI NIH HHS R21 HL110667NHLBI NIH HHS T32 HL007895NHLBI NIH HHS T32 HL069766NIGMS NIH HHS T32 GM007185
6 · The paper itself

Abstract

We previously reported a genetic analysis of heart failure traits in a population of inbred mouse strains treated with isoproterenol to mimic catecholamine-driven cardiac hypertrophy. Here, we apply a co-expression network algorithm, wMICA, to perform a systems-level analysis of left ventricular transcriptomes from these mice. We describe the features of the overall network but focus on a module identified in treated hearts that is strongly related to cardiac hypertrophy and pathological remodeling. Using the causal modeling algorithm NEO, we identified the gene Adamts2 as a putative regulator of this module and validated the predictive value of NEO using small interfering RNA-mediated knockdown in neonatal rat ventricular myocytes. Adamts2 silencing regulated the expression of the genes residing within the module and impaired isoproterenol-induced cellular hypertrophy. Our results provide a view of higher order interactions in heart failure with potential for diagnostic and therapeutic insights.

Indexed as

ADAMTS ProteinsAnimalsCardiomegalyCardiomyopathiesCardiotonic AgentsCatecholaminesGene Expression RegulationGene Regulatory NetworksHeart FailureHeart VentriclesIsoproterenolMiceMice, Inbred StrainsMyocardiumMyocytes, CardiacSignal TransductionAdamts2 protein, mouseADAMTS ProteinsCardiotonic AgentsCatecholaminesIsoproterenolcausal modelinggene networkMICAsiRNA mediated knockdownventricular myocytes

Identifiers

PMID27866946
PMCPMC5338604
OpenAlexW2550900176

What OpenQuestion holds

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Registered trials

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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.