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HDAC3 Impairs Cardiac Function in Chronic Heart Failure Rats via Mediating MicroRNA-26b-3p to Target High Mobility

Xinyuan Han1,2, Shunda Wang2, Zhijun Yong2

  • 1Department of Cardiovascular Medicine, The First Affiliated Hospital of Xi'an Jiaotong University, Xi'an, 710061, Shaanxi, China.

Current Medicinal Chemistry
|October 6, 2022
PubMed

Insights

Downregulating histone deacetylase 3 (HDAC3) improves heart function in chronic heart failure (CHF) rats by regulating the microRNA-26b-3p (miR-26b-3p)/high mobility group AT-hook 2 (HMGA2) axis. This offers new therapeutic strategies for CHF.

Area of Science:

  • Cardiovascular Biology
  • Molecular Medicine
  • Epigenetics

Background:

  • Chronic heart failure (CHF) involves complex regulatory mechanisms.
  • The role of histone deacetylase 3 (HDAC3) in CHF, particularly its regulation of the microRNA-26b-3p (miR-26b-3p)/high mobility group AT-hook 2 (HMGA2) axis, remains under-investigated.

Purpose of the Study:

  • To investigate the effects of HDAC3, miR-26b-3p, and HMGA2 on the development of CHF.
  • To elucidate the regulatory mechanism of HDAC3 on the miR-26b-3p/HMGA2 axis in CHF.

Main Methods:

  • Established rat models of CHF using aortic coarctation.
  • Quantified levels of HDAC3, miR-26b-3p, and HMGA2 in CHF rats.
  • Administered oligonucleotides and plasmids targeting HDAC3, miR-26b-3p, and HMGA2 to assess effects on cardiac function, inflammation, myocardial pathology, and cardiomyocyte apoptosis.
  • Validated the interaction between miR-26b-3p and HMGA2, and between HDAC3 and miR-26b-3p.

Main Results:

  • HDAC3 and HMGA2 levels were elevated, while miR-26b-3p was decreased in CHF rats.
  • Reduced HDAC3 or HMGA2, or increased miR-26b-3p, attenuated CHF progression, improving cardiac function and reducing inflammation and apoptosis.
  • Inhibition of miR-26b-3p or elevation of HMGA2 reversed the protective effects of HDAC3 downregulation.
  • Mechanistically, miR-26b-3p directly targets HMGA2, and HDAC3 interacts with miR-26b-3p.

Conclusions:

  • Downregulation of HDAC3 alleviates cardiac dysfunction in CHF rats by modulating the miR-26b-3p/HMGA2 axis.
  • This study provides novel theoretical insights and potential therapeutic targets for CHF treatment.
Abstract

Keywords:
Chronic heart failurecardiac functionfibrosishigh mobility group AT-hook 2histone deacetylase 3microRNA-26b-3p

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