Evidence map›Paper›PMID 18780759›Full record

ArticlePhysiological genomics2008

Key pathways associated with heart failure development revealed by gene networks correlated with cardiac remodeling.

Zhong Gao, Andreas S Barth, Deborah DiSilvestre, Fadi G Akar, Yanli Tian, Antti Tanskanen, David A Kass, Raimond L Winslow, Gordon F Tomaselli

Open access · greenAbstract read
In one paragraph

Article in Physiological genomics, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
2.8field-weighted citation impact, top 9% 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

27 citing papers in PubMed, 51 citations in OpenAlex.

  1. Review
  2. Article
  3. Implications for neutrophils in cardiac arrhythmias.American journal of physiology. Heart and circulatory physiology · 2024
    Review
  4. Review
  5. Article
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  15. Transcriptome, proteome, and metabolome in dyssynchronous heart failure and CRT.Journal of cardiovascular translational research · 2012
    Review
  16. Cellular electrophysiological abnormalities in dyssynchronous hearts and during CRT.Journal of cardiovascular translational research · 2012
    Review
  17. Metabolic stress, reactive oxygen species, and arrhythmia.Journal of molecular and cellular cardiology · 2012
    Review
  18. Review
  19. Deciphering Arrhythmia Mechanisms - Tools of the Trade.Cardiac electrophysiology clinics · 2011
    Article
  20. Review
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

9 authors at 1 institution in 1 country.

Zhong GaoThe Institute for Computational Medicine, The Johns Hopkins University, Baltimore, Maryland 21205, USA.
Andreas S Barth
Deborah DiSilvestre
Fadi G Akar
Yanli Tian
Antti Tanskanen
David A Kass
Raimond L Winslow
Gordon F Tomaselli
Johns Hopkins University · US

Funding

Pathobiology of Cardiac Dyssynchrony &ResynchronizationP01HL077180 · NHLBI · JOHNS HOPKINS UNIVERSITY · PI KASS, DAVID ALAN · 2004 to 2014
$22.8M
Expression Profiling in Canine Models of Human DiseaseR01HL072488 · NHLBI · JOHNS HOPKINS UNIVERSITY · PI TOMASELLI, GORDON FRANK · 2002 to 2005
$3.2M
NHLBI NIH HHS P01 HL-77180NHLBI NIH HHS R01 HL-72488
6 · The paper itself

Abstract

Heart failure (HF) is the leading cause of morbidity and mortality in the industrialized world. While the transcriptomic changes in end-stage failing myocardium have received much attention, no information is available on the gene expression patterns associated with the development of HF in large mammals. Therefore, we used a well-controlled canine model of tachycardia-induced HF to examine global gene expression in left ventricular myocardium with Affymetrix canine oligonucleotide arrays at various stages after initiation of rapid ventricular pacing (days 3, 7, 14, and 21). The gene expression data were complemented with measurements of action potential duration, conduction velocity, and left ventricular end diastolic pressure, and dP/dt(max) over the time course of rapid ventricular pacing. As a result, we present a phenotype-centered gene association network, defining molecular systems that correspond temporally to hemodynamic and electrical remodeling processes. Gene Ontology analysis revealed an orchestrated regulation of oxidative phosphorylation, ATP synthesis, cell signaling pathways, and extracellular matrix components, which occurred as early as 3 days after the initiation of ventricular pacing, coinciding with the early decline in left ventricular pump function and prolongation of action potential duration. The development of clinically overt left ventricular dysfunction was associated with few additional changes in the myocardial transcriptome. We conclude that the majority of tachypacing-induced transcriptional changes occur early after initiation of rapid ventricular pacing. As the transition to overt HF is characterized by few additional transcriptional changes, posttranscriptional modifications may be more critical in regulating myocardial structure and function during later stages of HF.

Indexed as

Gene Regulatory NetworksAction PotentialsAnimalsDisease Models, AnimalDogsGene Expression ProfilingHeart FailureMyocardiumOligonucleotide Array Sequence AnalysisSignal TransductionTachycardia, VentricularVentricular Remodeling

Identifiers

PMID18780759
PMCPMC2585017
OpenAlexW2109986216

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.