Evidence map›Paper›PMID 29288409›Full record

ArticleBasic research in cardiology2018

Gene expression analysis to identify mechanisms underlying heart failure susceptibility in mice and humans.

Christoph Koentges, Mark E Pepin, Carolyn Müsse, Katharina Pfeil, Sonia V Viteri Alvarez, Natalie Hoppe, Michael M Hoffmann, Katja E Odening, Samuel Sossalla, Andreas Zirlik and 4 more

Abstract readComparative Study
In one paragraph

Article in Basic research in cardiology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed, 1 pooled it
4.3field-weighted citation impact, top 4% 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

30 citing papers in PubMed, 1 synthesis or guideline pooled it, 43 citations in OpenAlex.

  1. Pooled it
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  12. Transcriptome studies of inherited dilated cardiomyopathies.Mammalian genome : official journal of the International Mammalian Genome Society · 2023
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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

14 authors at 3 institutions in 2 countries.

Christoph KoentgesCardiology and Angiology I, Heart Center, Freiburg University, Hugstetter Str. 55, 79106, Freiburg, Germany.
Mark E PepinDivision of Molecular and Cellular Pathology, Department of Pathology, University of Alabama at Birmingham, 901 19th Street South, BMR2 Rm 506, Birmingham, AL, 35294, USA.
Carolyn MüsseCardiology and Angiology I, Heart Center, Freiburg University, Hugstetter Str. 55, 79106, Freiburg, Germany.
Katharina PfeilCardiology and Angiology I, Heart Center, Freiburg University, Hugstetter Str. 55, 79106, Freiburg, Germany.
Sonia V Viteri AlvarezCardiology and Angiology I, Heart Center, Freiburg University, Hugstetter Str. 55, 79106, Freiburg, Germany.
Natalie HoppeCardiology and Angiology I, Heart Center, Freiburg University, Hugstetter Str. 55, 79106, Freiburg, Germany.
Michael M HoffmannFaculty of Medicine, University of Freiburg, Freiburg, Germany.
Katja E OdeningCardiology and Angiology I, Heart Center, Freiburg University, Hugstetter Str. 55, 79106, Freiburg, Germany.
Samuel SossallaDepartment of Internal Medicine II, University Hospital Regensburg, Regensburg, Germany.
Andreas ZirlikCardiology and Angiology I, Heart Center, Freiburg University, Hugstetter Str. 55, 79106, Freiburg, Germany.
Lutz HeinFaculty of Medicine, University of Freiburg, Freiburg, Germany.
Christoph BodeCardiology and Angiology I, Heart Center, Freiburg University, Hugstetter Str. 55, 79106, Freiburg, Germany.
Adam R WendeDivision of Molecular and Cellular Pathology, Department of Pathology, University of Alabama at Birmingham, 901 19th Street South, BMR2 Rm 506, Birmingham, AL, 35294, USA. adamwende@uabmc.edu.
Heiko BuggerCardiology and Angiology I, Heart Center, Freiburg University, Hugstetter Str. 55, 79106, Freiburg, Germany. heiko.bugger@universitaets-herzzentrum.de.
University of Freiburg · DEUniversity of Alabama at Birmingham · USUniversity Hospital Regensburg · DE

Funding

University of Alabama at Birmingham's Diabetes Research CenterP30DK079626 · NIDDK · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI BARBARA A GOWER · 2013 to 2026
$19.5M
Interdisciplinary Training in Pathobiology and Rehabilitation Medicine.T32HD071866 · NICHD · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI JAMES RIMMER, Anna E. Thalacker-Mercer · 2012 to 2026
$4.8M
The essentiality of serine and glycine for skeletal muscle regeneration in agingR01AG075059 · NIA · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI THALACKER-MERCER, ANNA E. · 2022 to 2025
$1.5M
Glucose-Mediated Remodeling of Cardiac DNA MethylationR01HL133011 · NHLBI · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI WENDE, ADAM RAYMOND · 2017 to 2020
$1.5M
Glucose-Mediated Remodeling of Cardiac DNA MethylationR56HL133011 · NHLBI · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI WENDE, ADAM RAYMOND · 2016 to 2016
$368k
Deutsche Forschungsgemeinschaft Bu2126/3-1NHLBI NIH HHS R01 HL133011NHLBI NIH HHS R56 HL133011NIA NIH HHS R01 AG075059NICHD NIH HHS T32 HD071866NIDDK NIH HHS P30 DK079626NIH HHS HL133011NIH HHS T32HD071866
6 · The paper itself

Abstract

Genetic factors are known to modulate cardiac susceptibility to ventricular hypertrophy and failure. To determine how strain influences the transcriptional response to pressure overload-induced heart failure (HF) and which of these changes accurately reflect the human disease, we analyzed the myocardial transcriptional profile of mouse strains with high (C57BL/6J) and low (129S1/SvImJ) susceptibility for HF development, which we compared to that of human failing hearts. Following transverse aortic constriction (TAC), C57BL/6J mice developed overt HF while 129S1/SvImJ did not. Despite a milder aortic constriction, impairment of ejection fraction and ventricular remodeling (dilation, fibrosis) was more pronounced in C57BL/6J mice. Similarly, changes in myocardial gene expression were more robust in C57BL/6J (461 genes) compared to 129S1/SvImJ mice (71 genes). When comparing these patterns to human dilated cardiomyopathy (1344 genes), C57BL/6J mice tightly grouped to human hearts. Overlay and bioinformatic analysis of the transcriptional profiles of C57BL/6J mice and human failing hearts identified six co-regulated genes (POSTN, CTGF, FN1, LOX, NOX4, TGFB2) with established link to HF development. Pathway enrichment analysis identified angiotensin and IGF-1 signaling as most enriched putative upstream regulator and pathway, respectively, shared between TAC-induced HF in C57BL/6J mice and in human failing hearts. TAC-induced heart failure in C57BL/6J mice more closely reflects the gene expression pattern of human dilated cardiomyopathy compared to 129S1/SvImJ mice. Unbiased as well as targeted gene expression and pathway analyses identified periostin, angiotensin signaling, and IGF-1 signaling as potential causes of increased HF susceptibility in C57BL/6J mice and as potentially useful drug targets for HF treatment.

Indexed as

Gene Expression RegulationAnimalsCardiomyopathy, DilatedCase-Control StudiesDisease Models, AnimalDisease ProgressionGene Expression ProfilingGene Regulatory NetworksGenetic Predisposition to DiseaseHeart FailureHypertrophy, Left VentricularMaleMice, 129 StrainMice, Inbred C57BLPhenotypeSpecies SpecificityCardiac functionGene expressionGenetic backgroundHeart failureTransverse aortic constriction

Identifiers

PMID29288409
PMCPMC5764079
OpenAlexW2776940606

What Socratic holds

Textmetadata
LicenceTDM
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 Socratic graph.