Evidence map›Paper›PMID 36004821›Full record

ReviewCardiovascular research2023

Emerging epigenetic therapies of cardiac fibrosis and remodelling in heart failure: from basic mechanisms to early clinical development.

Timothy A McKinsey, Roger Foo, Chukwuemeka George Anene-Nzelu, Joshua G Travers, Ronald J Vagnozzi, Natalie Weber, Thomas Thum

Open access · greenAbstract readReview
In one paragraph

Review in Cardiovascular research, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.

0numbers the graph read from it
0cells of the map it votes in
42citing papers in PubMed
5.2field-weighted citation impact, top 3% 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

42 citing papers in PubMed, 68 citations in OpenAlex.

  1. Review
  2. ETS‑1/ETS‑2 transcription factors in CVD (Review).International journal of molecular medicine · 2026
    Review
  3. Review
  4. Cardiac epigenome in heart development and disease.Nature reviews. Cardiology · 2026
    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

7 authors at 4 institutions in 4 countries.

Timothy A McKinseyDepartment of Medicine, Division of Cardiology, and Consortium for Fibrosis Research & Translation, University of Colorado Anschutz Medical Campus, 12700 E.19th Ave, Aurora, CO, 80045-2507, USA.
Roger FooNUHS Cardiovascular Disease Translational Research Programme, NUS Yong Loo Lin School of Medicine, 14 Medical Drive, Level 8, 117599 Singapore, Singapore.ORCID 0000-0002-8079-4618
Chukwuemeka George Anene-NzeluNUHS Cardiovascular Disease Translational Research Programme, NUS Yong Loo Lin School of Medicine, 14 Medical Drive, Level 8, 117599 Singapore, Singapore.
Joshua G TraversDepartment of Medicine, Division of Cardiology, and Consortium for Fibrosis Research & Translation, University of Colorado Anschutz Medical Campus, 12700 E.19th Ave, Aurora, CO, 80045-2507, USA.
Ronald J VagnozziDepartment of Medicine, Division of Cardiology, and Consortium for Fibrosis Research & Translation, University of Colorado Anschutz Medical Campus, 12700 E.19th Ave, Aurora, CO, 80045-2507, USA.
Natalie WeberInstitute of Molecular and Translational Therapeutic Strategies (IMTTS), Hannover Medical School, Carl-Neuberg-Straße 1, 30625 Hannover, Germany.
Thomas ThumInstitute of Molecular and Translational Therapeutic Strategies (IMTTS), Hannover Medical School, Carl-Neuberg-Straße 1, 30625 Hannover, Germany.ORCID 0000-0003-4360-1511
University of Colorado Anschutz Medical Campus · USMedizinische Hochschule Hannover · DEMontreal Heart Institute · CANational University Heart Centre Singapore · SG

Funding

Regulation of Cardiac Signaling by Class I Histone DeacetylasesR01HL116848 · NHLBI · UNIVERSITY OF COLORADO DENVER · PI MCKINSEY, TIMOTHY · 2013 to 2021
$3.1M
Exploring the Therapeutic Potential of BRD4 Extra-terminal Domain Inhibition in Cardiac Dysfunction and Remodeling. Fellow: Joshua TraversF32HL147463 · NHLBI · UNIVERSITY OF COLORADO DENVER · PI TRAVERS, JOSHUA · 2019 to 2020
$127k
NHLBI NIH HHS F32 HL147463NIH HHS HL116848
6 · The paper itself

Abstract

Cardiovascular diseases and specifically heart failure (HF) impact global health and impose a significant economic burden on society. Despite current advances in standard of care, the risks for death and readmission of HF patients remain unacceptably high and new therapeutic strategies to limit HF progression are highly sought. In disease settings, persistent mechanical or neurohormonal stress to the myocardium triggers maladaptive cardiac remodelling, which alters cardiac function and structure at both the molecular and cellular levels. The progression and magnitude of maladaptive cardiac remodelling ultimately leads to the development of HF. Classical therapies for HF are largely protein-based and mostly are targeted to ameliorate the dysregulation of neuroendocrine pathways and halt adverse remodelling. More recently, investigation of novel molecular targets and the application of cellular therapies, epigenetic modifications, and regulatory RNAs has uncovered promising new avenues to address HF. In this review, we summarize the current knowledge on novel cellular and epigenetic therapies and focus on two non-coding RNA-based strategies that reached the phase of early clinical development to counteract cardiac remodelling and HF. The current status of the development of translating those novel therapies to clinical practice, limitations, and future perspectives are additionally discussed.

Indexed as

Heart FailureVentricular RemodelingEpigenesis, GeneticFibrosisHumansMyocardiumEpigeneticsFibrosisHeart failureMicroRNAsNon-coding RNAs

Identifiers

PMID36004821
PMCPMC10202443
OpenAlexW4293090934

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.