Evidence map›Paper›PMID 24838003›Full record

ReviewJournal of molecular and cellular cardiology2014

BET-ting on chromatin-based therapeutics for heart failure.

Saptarsi M Haldar, Timothy A McKinsey

Open access · greenAbstract readReview
In one paragraph

Review in Journal of molecular and cellular cardiology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed, 1 pooled it
3.0field-weighted citation impact, top 8% 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

28 citing papers in PubMed, 1 synthesis or guideline pooled it, 48 citations in OpenAlex.

  1. Guideline
  2. Cell Type-Specific Roles for BRD4 in Heart Failure.Current cardiology reports · 2026
    Review
  3. Cardiac epigenome in heart development and disease.Nature reviews. Cardiology · 2026
    Review
  4. Review
  5. Article
  6. Article
  7. Article
  8. Review
  9. Review
  10. Article
  11. BET Protein-Mediated Transcriptional Regulation in Heart Failure.International journal of molecular sciences · 2021
    Review
  12. Article
  13. Review
  14. Epigenetic therapies in heart failure.Journal of molecular and cellular cardiology · 2019
    Article
  15. Article
  16. Epigenomes in Cardiovascular Disease.Circulation research · 2018
    Review
  17. Review
  18. Article
  19. Article
  20. Article
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

2 authors at 2 institutions in 1 country.

Saptarsi M HaldarCase Cardiovascular Research Institute, Department of Medicine, Case Western Reserve University School of Medicine, Cleveland, OH 44106, USA; Harrington Heart & Vascular Institute, University Hospitals Case Medical Center, Cleveland, OH 44106, USA. Electronic address: saptarsi.haldar@case.edu.
Timothy A McKinseyDepartment of Medicine, Division of Cardiology, University of Colorado Denver, Aurora, CO 80045, USA. Electronic address: timothy.mckinsey@ucdenver.edu.
University of Colorado Denver · USUniversity School · US

Funding

Regulation of Cardiac Signaling by Class I Histone DeacetylasesR01HL116848 · NHLBI · UNIVERSITY OF COLORADO DENVER · PI MCKINSEY, TIMOTHY · 2013 to 2021
$3.1M
KLF15 and Transcriptional Control of Muscle MetabolismR01DK093821 · NIDDK · J. DAVID GLADSTONE INSTITUTES · PI HALDAR, SAPTARSI · 2013 to 2017
$1.8M
Isoform-Selective HDAC Inhibitors for Age-Associated Diastolic DysfunctionR21AG043822 · NIA · UNIVERSITY OF COLORADO DENVER · PI MCKINSEY, TIMOTHY · 2012 to 2013
$414k
NHLBI NIH HHS HL116848NHLBI NIH HHS R01 HL116848NIA NIH HHS AG043822NIA NIH HHS R21 AG043822NIDDK NIH HHS DK093821NIDDK NIH HHS R01 DK093821
6 · The paper itself

Abstract

Studies of transcriptional mechanisms in heart failure have focused heavily on roles of sequence-specific DNA-binding factors such as NFAT, MEF2 and GATA4. Recent findings have illuminated crucial functions for epigenetic regulators in the control of cardiac structural remodeling and mechanical dysfunction in response to pathological stress. Here, we review the current understanding of chromatin-dependent signal transduction in cardiac gene control, and highlight the potential for pharmacologic regulation of BET acetyl-lysine binding proteins as a means of treating heart failure.

Indexed as

Epigenesis, GeneticBromodomain Containing ProteinsCardiomegalyCardiotonic AgentsCell Cycle ProteinsChromatinHeart FailureHumansNuclear ProteinsPositive Transcriptional Elongation Factor BRepressor ProteinsRNA-Binding ProteinsSignal TransductionTranscription FactorsTranscription, GeneticTumor Suppressor ProteinsBCL11B protein, humanBRD4 protein, humanBromodomain Containing ProteinsCardiotonic AgentsCell Cycle ProteinsChromatinHEXIM1 protein, humanNuclear ProteinsPositive Transcriptional Elongation Factor BRepressor ProteinsRNA-Binding ProteinsTranscription FactorsTumor Suppressor ProteinsBET proteinsCardiac hypertrophyChromatinEpigeneticsHeart failureTranscription

Identifiers

PMID24838003
PMCPMC4115033
OpenAlexW2045115744

What OpenQuestion 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 OpenQuestion graph.