ArticleJournal of molecular and cellular cardiology2018
HDAC1 localizes to the mitochondria of cardiac myocytes and contributes to early cardiac reperfusion injury.
Article in Journal of molecular and cellular cardiology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.
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Who cites it
44 citing papers in PubMed, 74 citations in OpenAlex.
- Lactylation: Metabolic epigenetic regulation and cell death mechanisms in myocardial ischemia‒reperfusion injury.Genes & diseases · 2027Review
- The histone deacetylase family in health and disease.Signal transduction and targeted therapy · 2026Review
- The Trajectory of Epigenetic Chromatin Remodeling in Cardiometabolic Disease and its Therapeutic Implications.Journal of cardiovascular translational research · 2026Review
- Zonal hepatocellular responses to acute ethanol consumption: impacts on mitochondrial function and liver metabolism.Toxicological sciences : an official journal of the Society of Toxicology · 2026Article
- Methylation-centric epigenetic regulation in dilated cardiomyopathy: mechanisms, metabolic interplay, and translational potential.Frontiers in cardiovascular medicine · 2026Review
- IDH2 lactylation promotes angiogenesis in murine diabetic myocardial infarction via blocking Cav1-eNOS interaction.Nature communications · 2025Article
- Role of Histone Deacetylase and Inhibitors in Cardiovascular Diseases.Cell proliferation · 2025Review
- Unlocking cardiac health: exploring the role of class I HDACs in cardiovascular diseases.Molecular and cellular biochemistry · 2025Review
- The Role of HINT3 in Myocardial Ischemia-Reperfusion Injury in Male Mice: Mechanisms Involving SDHA and its Acetylation.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- HDACs and Their Inhibitors on Post-Translational Modifications: The Regulation of Cardiovascular Disease.Cells · 2025Review
- Emerging Epigenetic Therapies for the Treatment of Cardiac Fibrosis.Biomedicines · 2025Review
- Comprehensive analysis of diagnostic biomarkers related to histone acetylation in acute myocardial infarction.BMC medical genomics · 2025Article
- Mitochondrial KMT9 methylates DLAT to control pyruvate dehydrogenase activity and prostate cancer growth.Nature communications · 2025Article
- Downregulation of Gldc attenuates myocardial ischemia reperfusion injury in vitro by modulating Akt and NF-κB signalings.Scientific reports · 2025Article
- MitoTracker Red for isolation of zone-specific hepatocytes and characterization of hepatic sublobular metabolism.Biochemical and biophysical research communications · 2024Article
- Autotaxin Inhibition Reduces Post-Ischemic Myocardial Inflammation via Epigenetic Gene Modifications.Stem cell reviews and reports · 2024Article
- Review
- The role of acetylation in obesity-induced cardiac metabolic alterations.Journal of pharmacy & pharmaceutical sciences : a publication of the Canadian Society for Pharmaceutical Sciences, Societe canadienne des sciences pharmaceutiques · 2024Review
- LP342, a novel histone deacetylase inhibitor, decreases nitro-oxidative stress, mitochondrial dysfunction and hepatic ischaemia/reperfusion injury in mice.RPS pharmacy and pharmacology reports · 2023Article
- Article
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
Abstract
rationaleRecent evidence indicates that histone deacetylase enzymes (HDACs) contribute to ischemia reperfusion (I/R) injury, and pan-HDAC inhibitors have been shown to be cardioprotective when administered either before an ischemic insult or during reperfusion. We have shown previously that selective inhibition of class I HDACs provides superior cardioprotection when compared to pan-HDAC inhibition in a pretreatment model, but selective class I HDAC inhibition has not been tested during reperfusion, and specific targets of class I HDACs in I/R injury have not been identified.
objectiveWe hypothesized that selective inhibition of class I HDACs with the drug MS-275 (entinostat) during reperfusion would improve recovery from I/R injury in the first hour of reperfusion. METHODS AND
resultsHearts from male Sprague-Dawley rats were subjected to ex vivo I/R injury±MS-275 class I HDAC inhibition during reperfusion alone. MS-275 significantly attenuated I/R injury, as indicated by improved LV function and tissue viability at the end of reperfusion. Unexpectedly, we observed that HDAC1 is present in the mitochondria of cardiac myocytes, but not fibroblasts or endothelial cells. We then designed mitochondria-restricted and mitochondria-excluded HDAC inhibitors, and tested both in our ex vivo I/R model. The selective inhibition of mitochondrial HDAC1 attenuated I/R injury to the same extent as MS-275, whereas the mitochondrial-excluded inhibitor did not. Further assays demonstrated that these effects are attributable to a decrease in SDHA activity and subsequent metabolic ROS production in reperfusion.
conclusionsWe demonstrate for the first time that HDAC1 is present within the mitochondria of cardiac myocytes, and mitochondrial HDAC1 contributes significantly to I/R injury within the first hour of reperfusion.
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