Evidence map›Paper›PMID 25992271›Full record

ReviewPulmonary circulation2015

Emerging roles for histone deacetylases in pulmonary hypertension and right ventricular remodeling (2013 Grover Conference series).

Maria A Cavasin, Kurt R Stenmark, Timothy A McKinsey

Open access · bronzeAbstract readReview
In one paragraph

Review in Pulmonary circulation, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed, 1 pooled it
1.7field-weighted citation impact, top 16% 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

23 citing papers in PubMed, 1 synthesis or guideline pooled it, 33 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Review
  4. Review
  5. Review
  6. Review
  7. Review
  8. Article
  9. Review
  10. Review
  11. The DNA Damage Response and HIV-Associated Pulmonary Arterial Hypertension.International journal of molecular sciences · 2020
    Review
  12. Article
  13. Article
  14. MEF2 and the Right Ventricle: From Development to Disease.Frontiers in cardiovascular medicine · 2019
    Review
  15. Insights on the epigenetic mechanisms underlying pulmonary arterial hypertension.Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologica · 2018
    Review
  16. Review
  17. Review
  18. Review
  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

3 authors at 1 institution in 1 country.

Maria A CavasinDepartment of Medicine, Division of Cardiology, University of Colorado Denver, Aurora, Colorado, USA.
Kurt R StenmarkDepartment of Pediatrics, Division of Pulmonary and Critical Care Medicine, University of Colorado Denver, Aurora, Colorado, USA.
Timothy A McKinseyDepartment of Medicine, Division of Cardiology, University of Colorado Denver, Aurora, Colorado, USA.
University of Colorado Denver · US

Funding

VRAC and Rho in pulmonary EC proliferationP01HL014985 · NHLBI · UNIVERSITY OF COLORADO DENVER · PI STENMARK, KURT R. · 1985 to 2019
$35.1M
Fibroblasts and Mononuclear Fibrogenic Cells Drive Right Ventricular Pulmonary ArR01HL114887 · NHLBI · UNIVERSITY OF COLORADO DENVER · PI BULL, TODD M, BUTTRICK, PETER N. · 2012 to 2016
$3.4M
Regulation of Cardiac Signaling by Class I Histone DeacetylasesR01HL116848 · NHLBI · UNIVERSITY OF COLORADO DENVER · PI MCKINSEY, TIMOTHY · 2013 to 2021
$3.1M
NHLBI NIH HHS P01 HL014985NHLBI NIH HHS R01 HL114887NHLBI NIH HHS R01 HL116848
6 · The paper itself

Abstract

Reversible lysine acetylation has emerged as a critical mechanism for controlling the function of nucleosomal histones as well as diverse nonhistone proteins. Acetyl groups are conjugated to lysine residues in proteins by histone acetyltransferases and removed by histone deacetylases (HDACs), which are also commonly referred to as lysine deacetylases. Over the past decade, many studies have shown that HDACs play crucial roles in the control of left ventricular (LV) cardiac remodeling in response to stress. Small molecule HDAC inhibitors block pathological hypertrophy and fibrosis and improve cardiac function in various preclinical models of LV failure. Only recently have HDACs been studied in the context of right ventricular (RV) failure, which commonly occurs in patients who experience pulmonary hypertension (PH). Here, we review recent findings with HDAC inhibitors in models of PH and RV remodeling, propose next steps for this newly uncovered area of research, and highlight potential for isoform-selective HDAC inhibitors for the treatment of PH and RV failure.

Indexed as

epigeneticshistone deacetylasespulmonary hypertensionright ventricle

Identifiers

PMID25992271
PMCPMC4405717
OpenAlexW2069373787

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.