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J Mol Cell Cardiol. 2019 Apr;129:188-192. doi: 10.1016/j.yjmcc.2019.02.013. Epub 2019 Feb 27.

HDAC inhibition as a therapeutic strategy in myocardial ischemia/reperfusion injury.

Author information

1
Department of Medicine, Division of Cardiovascular Disease, The University of Alabam at Birmingham, Birmingham, AL 35233, United States of America. Electronic address: mxie@uabmc.edu.
2
Department of Internal Medicine, Fuwai Hospital, Chinese Academy for Medical Science, National Center of Cardiovascular Disease, Beijing 100037, China.
3
Department of Internal Medicine, Division of Cardiology, UT Southwestern Medical Center, 6000 Harry Hines Blvd. NB11.200, Dallas, United States of America; Department of Molecular Biology, UT Southwestern Medical Center, 6000 Harry Hines Blvd. NB11.200, Dallas, United States of America.

Abstract

Reperfusion injury during myocardial infarction accounts for approximately half of final infarct size. Whereas this has been known for decades, efficacious therapy targeting reperfusion injury remains elusive. Many proteins are subject to reversible acetylation, and drugs targeting enzymes that govern these events have emerged in oncology. Among these, small molecules targeting protein deacetylating enzymes, so-called histone deacetylases (HDACs), are approved for human use in rare cancers. Now, work emerging from multiple laboratories, and in both mice and large animals, has documented that HDAC inhibition using compounds approved for clinical use confers robust cardioprotection when delivered at the time of myocardial reperfusion. Here, we summarize the key underpinnings of this science, discuss potential mechanisms, and provide a framework for a first-in-human clinical trial.

PMID:
30825484
PMCID:
PMC6486856
[Available on 2020-04-01]
DOI:
10.1016/j.yjmcc.2019.02.013

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