Evidence map›Paper›PMID 23762381›Full record

ArticlePloS one2013

HDAC inhibition elicits myocardial protective effect through modulation of MKK3/Akt-1.

Ting C Zhao, Jianfeng Du, Shougang Zhuang, Shugang Zhuang, Paul Liu, Ling X Zhang

Erratum issuedOpen access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 26 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed, 1 pooled it
1.2field-weighted citation impact, top 21% 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

26 citing papers in PubMed, 1 synthesis or guideline pooled it, 31 citations in OpenAlex.

  1. Pooled it
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  13. Histone acetylation and DNA methylation in ischemia/reperfusion injury.Clinical science (London, England : 1979) · 2019
    Review
  14. Article
  15. Histones and heart failure in diabetes.Cellular and molecular life sciences : CMLS · 2018
    Review
  16. Article
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4 · The record

Corrections and comments

  • Erratum issued
    Zhuang, Shugang [corrected to Zhuang, Shougang]
5 · Who and what money

Authors and funding

6 authors at 3 institutions in 1 country.

Ting C ZhaoCardiovascular Research laboratory, Department of Surgery, Roger Williams Medical Center, Boston University Medical School, Providence, Rhode Island, United States of America. tzhao@bu.edu
Jianfeng Du
Shougang Zhuang
Shugang Zhuang
Paul Liu
Ling X Zhang
Rhode Island Hospital · USProvidence College · USRoger Williams Medical Center · US

Funding

Histone Deacetylase Inhibition: A Novel Approach to CardioprotectionR01HL089405 · NHLBI · ROGER WILLIAMS MEDICAL CENTER · PI ZHAO, TING C · 2009 to 2020
$3.4M
NHLBI NIH HHS R01 HL089405
6 · The paper itself

Abstract

We and others have demonstrated that HDAC inhibition protects the heart against myocardial injury. It is known that Akt-1 and MAP kinase play an essential role in modulation of myocardial protection and cardiac preconditioning. Our recent observations have shown that Akt-1 was activated in post-myocardial infarction following HDAC inhibition. However, it remains unknown whether MKK3 and Akt-1 are involved in HDAC inhibition-induced myocardial protection in acute myocardial ischemia and reperfusion injury. We sought to investigate whether the genetic disruption of Akt-1 and MKK3 eliminate cardioprotection elicited by HDAC inhibition and whether Akt-1 is associated with MKK3 to ultimately achieve protective effects. Adult wild type and MKK3⁻/⁻, Akt-1⁻/⁻ mice received intraperitoneal injections of trichostatin A (0.1 mg/kg), a potent inhibitor of HDACs. The hearts were subjected to 30 min myocardial ischemia/30 min reperfusion in the Langendorff perfused heart after twenty four hours to elicit pharmacologic preconditioning. Left ventricular function was measured, and infarct size was determined. Acetylation and phosphorylation of MKK3 were detected and disruption of Akt-1 abolished both acetylation and phosphorylation of MKK3. HDAC inhibition produces an improvement in left ventricular functional recovery, but these effects were abrogated by disruption of either Akt-1 or MKK3. Disruption of Akt-1 or MKK3 abolished the effects of HDAC inhibition-induced reduction of infarct size. Trichostatin A treatment resulted in an increase in MKK3 phosphorylation or acetylation in myocardium. Taken together, these results indicate that stimulation of the MKK3 and Akt-1 pathway is a novel approach to HDAC inhibition -induced cardioprotection.

Indexed as

AcetylationAnimalsBlotting, WesternFluorescent Antibody TechniqueHistone Deacetylase InhibitorsHistone DeacetylasesHydroxamic AcidsImmunoenzyme TechniquesImmunoprecipitationMaleMAP Kinase Kinase 3MiceMice, KnockoutMyocardial InfarctionPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktHistone Deacetylase InhibitorsHistone DeacetylasesHydroxamic AcidsMap2k3 protein, mouseMAP Kinase Kinase 3Phosphatidylinositol 3-KinasesProto-Oncogene Proteins c-akttrichostatin A

Identifiers

PMID23762381
PMCPMC3677871
OpenAlexW2113734956

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.