Evidence map›Paper›PMID 25159852›Full record

ArticlePhysiological genomics2014

Dynamic gene expression patterns in animal models of early and late heart failure reveal biphasic-bidirectional transcriptional activation of signaling pathways.

Janelle Rowell, Norimichi Koitabashi, David A Kass, Andreas S Barth

Abstract read
In one paragraph

Article in Physiological genomics, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.6field-weighted citation impact, top 18% 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

16 citing papers in PubMed, 27 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Deletion of cardiac polycystin 2/PC2 results in increased SR calcium release and blunted adrenergic reserve.American journal of physiology. Heart and circulatory physiology · 2020
    Article
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  6. Article
  7. AAV9-Molecular therapy. Methods & clinical development · 2019
    Article
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  9. Review
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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

4 authors at 1 institution in 1 country.

Janelle RowellDepartment of Medicine, Division of Cardiology, The Johns Hopkins Medical Institutions, Baltimore, Maryland.
Norimichi KoitabashiDepartment of Medicine, Division of Cardiology, The Johns Hopkins Medical Institutions, Baltimore, Maryland.
David A KassDepartment of Medicine, Division of Cardiology, The Johns Hopkins Medical Institutions, Baltimore, Maryland.
Andreas S BarthDepartment of Medicine, Division of Cardiology, The Johns Hopkins Medical Institutions, Baltimore, Maryland abarth3@jhmi.edu.
Johns Hopkins University · US

Funding

Training Program in Cellular and Molecular MedicineT32GM008752 · NIGMS · JOHNS HOPKINS UNIVERSITY · PI RAO, RAJINI · 2000 to 2019
$11.7M
Regulation and function of cGMP dependent protein kinase in cardiac hypertrophyR01HL093432 · NHLBI · JOHNS HOPKINS UNIVERSITY · PI TAKIMOTO, EIKI · 2009 to 2013
$2.3M
PKG Redox Modulation of Cardiac Function and DiseaseR01HL119012 · NHLBI · JOHNS HOPKINS UNIVERSITY · PI KASS, DAVID ALAN · 2013 to 2016
$1.6M
NHLBI NIH HHS HL-119012NHLBI NIH HHS HL-93432NIGMS NIH HHS T32 GM008752
6 · The paper itself

Abstract

Altered cardiac gene expression in heart failure (HF) has mostly been identified by single-point analysis of end-stage disease. This may miss earlier changes in gene expression that are transient and/or directionally opposite to those observed later. Myocardial datasets from the largest microarray data repository (Gene Expression Omnibus) yielded six HF studies with time-course data. Differentially expressed transcripts between nonfailing controls, early HF (<3 days after cardiac insult) and late HF (usually >2 wk) were determined, and analysis of KEGG pathways and predicted regulatory control elements performed. We found that gene expression followed varying patterns: Downregulation of metabolic pathways occurred early and was sustained into late-stage HF. In contrast, most signaling pathways undergo a complex biphasic pattern: Calcium signaling, p53, apoptosis, and MAPK pathways displayed a bidirectional response, declining early but rising late. These profiles were compatible with specific microRNA (miRNA) and transcription regulators: Estrogen-related receptor-α and myocyte-enhancer factor-2 binding sites were overrepresented in the promoter regions of downregulated transcripts. Concurrently, there were overrepresented binding sites for E2f and ETS family members (E-Twenty Six, including Gabp, Elf1, and Ets2), serum response and interferon regulated factor in biphasic-bidirectional and late-upregulated transcripts. Binding sites for miRNAs downregulated by HF were more common in upregulated transcripts (e.g., miRNA-22,-133a/b, and -150 in early HF and miRNA-1,-9,-499 in late HF). During the development of HF, gene expression is characterized by dynamic overlapping sets of transcripts controlled by specific interrelated regulatory mechanisms. While metabolic gene classes show early and sustained downregulation in HF, signaling pathways undergo a complex biphasic pattern with early down- and more pronounced late upregulation.

Indexed as

Gene Expression RegulationAnimalsBinding SitesDisease Models, AnimalDown-RegulationHeart FailureHumansMetabolic Networks and PathwaysMice, Inbred C57BLModels, CardiovascularSignal TransductionTime FactorsTranscriptional ActivationTranscription FactorsTranscriptomeUp-RegulationTranscription Factorsgene expressiongenomicsheart failuremeta-analysissignaling pathways

Identifiers

PMID25159852
PMCPMC4200378
OpenAlexW2012595264

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.