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Myocyte-specific overexpressing HDAC4 promotes myocardial ischemia/reperfusion injury

Ling Zhang1, Hao Wang2, Yu Zhao2

  • 1Department of Emergency Medicine, Department of Medicine, Rhode Island Hospital, Brown University, Providence, RI, USA.

Molecular Medicine (Cambridge, Mass.)
|August 24, 2018
PubMed

Insights

Activated histone deacetylase 4 (HDAC4) worsens heart injury after ischemia and reperfusion. Inhibiting HDAC4 may protect the heart, highlighting its role in cardiac protection and survival.

Area of Science:

  • Cardiovascular Biology
  • Molecular Cardiology
  • Cellular Signaling

Background:

  • Histone deacetylases (HDACs) are crucial for heart protection and cardiomyocyte survival.
  • The specific roles of HDAC isoforms in myocardial ischemia/reperfusion (I/R) injury are not fully understood.

Purpose of the Study:

  • To investigate the functional role of activated HDAC4 in mediating myocardial I/R injury.
  • To determine the impact of cardiomyocyte-specific active HDAC4 overexpression on cardiac function and survival.

Main Methods:

  • Developed myocyte-specific active HDAC4 transgenic mice.
  • Assessed ventricular function in isovolumetric perfused hearts.
  • Quantified infarct size using tetrazolium chloride staining.

Main Results:

  • Overexpression of active HDAC4 exacerbated myocardial I/R injury, increasing infarct size and reducing ventricular functional recovery.
  • Active HDAC4 increased markers of cell death (LC-3, active caspase 3) and decreased antioxidant defense (SOD-1).
  • Chemical HDAC inhibition mitigated the detrimental effects of active HDAC4.

Conclusions:

  • Activated HDAC4 is a critical regulator of myocardial ischemia and reperfusion injury.
  • Targeting HDAC4 activity may offer a therapeutic strategy for protecting the heart against I/R injury.
Abstract

Keywords:
Histone deacetylase4 (HDAC4)Ischemia/reperfusionMyocardial function

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