Language
English
Publication Date
1-1-2024
Journal
Frontiers in Physiology
DOI
10.3389/fphys.2024.1405569
PMID
38983721
PMCID
PMC11232433
PubMedCentral® Posted Date
6-24-2024
PubMedCentral® Full Text Version
Post-print
Abstract
Histone deacetylases (HDAC) catalyze the removal of acetylation modifications on histones and non-histone proteins, which regulates gene expression and other cellular processes. HDAC inhibitors (HDACi), approved anti-cancer agents, emerge as a potential new therapy for heart diseases. Cardioprotective effects of HDACi are observed in many preclinical animal models of heart diseases. Genetic mouse models have been developed to understand the role of each HDAC in cardiac functions. Some of the findings are controversial. Here, we provide an overview of how HDACi and HDAC impact cardiac functions under physiological or pathological conditions. We focus on in vivo studies of zinc-dependent classical HDACs, emphasizing disease conditions involving cardiac hypertrophy, myocardial infarction (MI), ischemic reperfusion (I/R) injury, and heart failure. In particular, we review how non-biased omics studies can help our understanding of the mechanisms underlying the cardiac effects of HDACi and HDAC.
Keywords
histone deacetylase, histone deacetylase inhibitor, cardiac hypertrophy, myocardial infarction, ischemic reperfusion, heart failure, genetic mouse models, multi-omics
Published Open-Access
yes
Recommended Citation
, "Targeting Histone Deacetylase in Cardiac Diseases" (2024). Faculty, Staff and Students Publications. 1134.
https://digitalcommons.library.tmc.edu/baylor_docs/1134