Evidence map›Paper›PMID 25791169›Full record

ReviewJournal of molecular and cellular cardiology2015

Non-sirtuin histone deacetylases in the control of cardiac aging.

Bradley S Ferguson, Timothy A McKinsey

Open access · greenAbstract readReview
In one paragraph

Review in Journal of molecular and cellular cardiology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
4.2field-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

27 citing papers in PubMed, 51 citations in OpenAlex.

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  16. The effect of melatonin on cardio fibrosis in juvenile rats with pressure overload and deregulation of HDACs.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2018
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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

2 authors at 1 institution in 1 country.

Bradley S FergusonDepartment of Medicine, Division of Cardiology, University of Colorado, Denver, 12700 E. 19th Ave Aurora, CO 80045-0508, USA.
Timothy A McKinseyDepartment of Medicine, Division of Cardiology, University of Colorado, Denver, 12700 E. 19th Ave Aurora, CO 80045-0508, USA. 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
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
Isoform-Selective HDAC Inhibitors for Age-Associated Diastolic DysfunctionR21AG043822 · NIA · UNIVERSITY OF COLORADO DENVER · PI MCKINSEY, TIMOTHY · 2012 to 2013
$414k
Role of dual-specificity phosphatase 5 (DUSP5) in the regulation of right ventricF32HL124893 · NHLBI · UNIVERSITY OF COLORADO DENVER · PI FERGUSON, BRADLEY S · 2014 to 2015
$77k
NHLBI NIH HHS 1F32HL124893-01NHLBI NIH HHS F32 HL124893NHLBI NIH HHS HL114887NHLBI NIH HHS HL116848NHLBI NIH HHS R01 HL114887NHLBI NIH HHS R01 HL116848NHLBI NIH HHS R01 HL127240NHLBI NIH HHS T32 HL007171NIA NIH HHS AG043822NIA NIH HHS R21 AG043822
6 · The paper itself

Abstract

Histone deacetylases (HDACs) catalyze the removal of acetyl-groups from lysine residues within nucelosomal histone tails and thousands of non-histone proteins. The 18 mammalian HDACs are grouped into four classes. Classes I, II and IV HDACs employ zinc as a co-factor for catalytic activity, while class III HDACs (also known as sirtuins) require NAD+ for enzymatic function. Small molecule inhibitors of zinc-dependent HDACs are efficacious in multiple pre-clinical models of pressure overload and ischemic cardiomyopathy, reducing pathological hypertrophy and fibrosis, and improving contractile function. Emerging data have revealed numerous mechanisms by which HDAC inhibitors benefit the heart, including suppression of oxidative stress and inflammation, inhibition of MAP kinase signaling, and enhancement of cardiac protein aggregate clearance and autophagic flux. Here, we summarize recent findings with zinc-dependent HDACs and HDAC inhibitors in the heart, focusing on newly described functions for distinct HDAC isoforms (e.g. HDAC2, HDAC3 and HDAC6). Potential for pharmacological HDAC inhibition as a means of treating age-related cardiac dysfunction is also discussed. This article is part of a Special Issue entitled: CV Aging.

Indexed as

Protein Processing, Post-TranslationalAgingAnimalsCardiomegalyHeart FailureHistone Deacetylase InhibitorsHistone DeacetylasesHistonesHumansInflammationIsoenzymesMyocardiumOxidative StressSignal TransductionHistone Deacetylase InhibitorsHistone DeacetylasesHistonesIsoenzymesAgingHeart failureHistone deacetylase

Identifiers

PMID25791169
PMCPMC4459895
OpenAlexW2089143221

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.