Evidence map›Paper›PMID 26876451›Full record

ReviewJournal of molecular and cellular cardiology2016

Epigenetic regulation of cardiac fibrosis.

Matthew S Stratton, Timothy A McKinsey

Abstract readReview
In one paragraph

Review in Journal of molecular and cellular cardiology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed, 1 pooled it
4.4field-weighted citation impact, top 5% 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

39 citing papers in PubMed, 1 synthesis or guideline pooled it, 62 citations in OpenAlex.

  1. Pooled it
  2. Herbacetin as a novel therapeutic agent for pulmonary and renal fibrosis by targeting TGFBR2 for degradation.Molecular therapy : the journal of the American Society of Gene Therapy · 2026
    Article
  3. Article
  4. Review
  5. Review
  6. Review
  7. Review
  8. Review
  9. Article
  10. Review
  11. Loss of Elmsan1 in cardiomyocytes leads to age-dependent cardiac dysfunction and reduced lifespan.American journal of physiology. Heart and circulatory physiology · 2025
    Article
  12. Review
  13. Article
  14. Bioactive Compounds and Cardiac Fibrosis: Current Insight and Future Prospect.Journal of cardiovascular development and disease · 2023
    Review
  15. Article
  16. Article
  17. Article
  18. Review
  19. 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

2 authors at 1 institution in 1 country.

Matthew S StrattonDepartment of Medicine, Division of Cardiology and Center for Fibrosis Research and Translation, University of Colorado Denver, 12700 E. 19th Ave, Aurora, CO 80045-0508, United States.
Timothy A McKinseyDepartment of Medicine, Division of Cardiology and Center for Fibrosis Research and Translation, University of Colorado Denver, 12700 E. 19th Ave, Aurora, CO 80045-0508, United States. Electronic address: timothy.mckinsey@ucdenver.edu.
University of Colorado Denver · US

Funding

Translational Pulmonary Vascular Biology ProgramT32HL007171 · NHLBI · UNIVERSITY OF COLORADO DENVER · PI Sonia Castro Flores, Tim Lahm · 1985 to 2026
$9.4M
Regulation of Chromatin Signaling in Heart Failure by the BRD4 Bromodomain Protein.R01HL127240 · NHLBI · UNIVERSITY OF COLORADO DENVER · PI MCKINSEY, TIMOTHY, SRIVASTAVA, DEEPAK · 2015 to 2022
$6.4M
POSTGRADUATE TRAINING IN CARDIOVASCULAR RESEARCHT32HL007822 · NHLBI · UNIVERSITY OF COLORADO DENVER · PI BUTTRICK, PETER N., LEINWAND, LESLIE ANNE · 1996 to 2023
$6.2M
Regulation of Cardiac Signaling by Class I Histone DeacetylasesR01HL116848 · NHLBI · UNIVERSITY OF COLORADO DENVER · PI MCKINSEY, TIMOTHY · 2013 to 2021
$3.1M
Isoform-Selective HDAC Inhibitors for Age-Associated Diastolic DysfunctionR21AG043822 · NIA · UNIVERSITY OF COLORADO DENVER · PI MCKINSEY, TIMOTHY · 2012 to 2013
$414k
Role of BET proteins in cardiac remodelingF32HL126354 · NHLBI · UNIVERSITY OF COLORADO DENVER · PI STRATTON, MATTHEW · 2015 to 2015
$54k
NHLBI NIH HHS 5T32HL007822NHLBI NIH HHS F32 HL126354NHLBI NIH HHS F32HL126354NHLBI NIH HHS HL116848NHLBI NIH HHS HL127240NHLBI NIH HHS R01 HL116848NHLBI NIH HHS R01 HL127240NHLBI NIH HHS T32 HL007171NHLBI NIH HHS T32 HL007822NIA NIH HHS AG043822NIA NIH HHS R21 AG043822
6 · The paper itself

Abstract

Fibrosis is defined as excess deposition of extracellular matrix (ECM), resulting in tissue scarring and organ dysfunction. In the heart, fibrosis may be reparative, replacing areas of myocyte loss with a structural scar following infarction, or reactive, which is triggered in the absence of cell death and involves interstitial ECM deposition in response to long-lasting stress. Interstitial fibrosis can increase the passive stiffness of the myocardium, resulting in impaired relaxation and diastolic dysfunction. Additionally, fibrosis can lead to disruption of electrical conduction in the heart, causing arrhythmias, and can limit myocyte oxygen availability and thus exacerbate myocardial ischemia. Here, we review recent studies that have illustrated key roles for epigenetic events in the control of pro-fibrotic gene expression, and highlight the potential of small molecules that target epigenetic regulators as a means of treating fibrotic cardiac diseases.

Indexed as

Epigenesis, GeneticExtracellular MatrixFibrosisHeart FailureHumansMyocardiumCardiacEpigeneticsFibrosis

Identifiers

PMID26876451
PMCPMC4987078
OpenAlexW2267545833

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.