Evidence map›Paper›PMID 30972522›Full record

ReviewHeart failure reviews2019

Targeting transcriptional machinery to inhibit enhancer-driven gene expression in heart failure.

Rachel A Minerath, Duane D Hall, Chad E Grueter

Open access · greenAbstract readReview
In one paragraph

Review in Heart failure reviews, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
0.4field-weighted citation impact, top 39% 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

8 citing papers in PubMed, 9 citations in OpenAlex.

  1. Exercise-induced cardiac hypertrophy: cellular and molecular mechanisms of cardiac adaptation following physical activity.Postepy w kardiologii interwencyjnej = Advances in interventional cardiology · 2026
    Review
  2. Article
  3. Article
  4. Review
  5. Dark DNA and stress (Review).International journal of molecular medicine · 2023
    Article
  6. Article
  7. Article
  8. 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

3 authors at 1 institution in 1 country.

Rachel A MinerathDepartment of Internal Medicine, Division of Cardiovascular Medicine, Francois M. Abboud Cardiovascular Research Center, Fraternal Order of Eagles Diabetes Research Center, University of Iowa, 169 Newton Rd., 4332 PBDB, Iowa City, IA, 52242, USA.
Duane D HallDepartment of Internal Medicine, Division of Cardiovascular Medicine, Francois M. Abboud Cardiovascular Research Center, Fraternal Order of Eagles Diabetes Research Center, University of Iowa, 169 Newton Rd., 4332 PBDB, Iowa City, IA, 52242, USA.
Chad E GrueterDepartment of Internal Medicine, Division of Cardiovascular Medicine, Francois M. Abboud Cardiovascular Research Center, Fraternal Order of Eagles Diabetes Research Center, University of Iowa, 169 Newton Rd., 4332 PBDB, Iowa City, IA, 52242, USA. chad-grueter@uiowa.edu.ORCID http://orcid.org/0000-0001-8950-742X
University of Iowa · US

Funding

MED13 Regulation of Cardiac Transcription in Obesity and HypothyroidismR01HL125436 · NHLBI · UNIVERSITY OF IOWA · PI GRUETER, CHAD E · 2015 to 2019
$1.9M
NHLBI NIH HHS R01 HL125436NHLBI NIH HHS R01-HL-125436
6 · The paper itself

Abstract

Pathological cardiac remodeling is induced through multiple mechanisms that include neurohumoral and biomechanical stress resulting in transcriptional alterations that ultimately become maladaptive and lead to the development of heart failure (HF). Although cardiac transcriptional remodeling is mediated by the activation of numerous signaling pathways that converge on a limited number of transcription factors (TFs) that promote hypertrophy (pro-hypertrophic TFs), the current therapeutic approach to prevent HF utilizes pharmacological inhibitors that largely target specific receptors that are activated in response to pathological stimuli. Thus, there is limited efficacy with the current pharmacological approaches to inhibit transcriptional remodeling associated with the development of HF. Recent evidence suggests that these pro-hypertrophic TFs co-localize at enhancers to cooperatively activate transcription associated with pathological cardiac remodeling. In disease states, including cancer and HF, evidence suggests that the general transcriptional machinery is disproportionately bound at enhancers. Therefore, pharmacological inhibition of transcriptional machinery that integrates pro-hypertrophic TFs may represent a promising alternative therapeutic approach to limit pathological remodeling associated with the development of HF.

Indexed as

AnimalsAtrial RemodelingCardiomegalyCyclin-Dependent KinasesGene Expression RegulationHeart FailureHumansMiceMolecular Targeted TherapyRNA, Long NoncodingSignal TransductionTranscription FactorsTranscription, GeneticVentricular RemodelingCyclin-Dependent KinasesRNA, Long NoncodingTranscription FactorsEnhancersEpigeneticsHeart failureTranscription

Identifiers

PMID30972522
PMCPMC6698214
OpenAlexW2937194911

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.