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Novel heart failure therapy targeting transcriptional pathway in cardiomyocytes by a natural compound, curcumin

Tatsuya Morimoto1, Yoichi Sunagawa, Masatoshi Fujita

  • 1Division of Molecular Medicine, School of Pharmaceutical Sciences, University of Shizuoka, Shizuoka, Japan. morimoto@u-shizuoka-ken.ac.jp

Circulation Journal : Official Journal of the Japanese Circulation Society
|May 15, 2010
PubMed

Insights

Curcumin may treat heart failure by inhibiting excessive histone acetylation in cardiomyocytes, a hallmark of maladaptive hypertrophy. This natural compound offers a safe and inexpensive therapeutic avenue for heart failure (HF).

Area of Science:

  • Cardiovascular disease
  • Molecular biology
  • Epigenetics

Background:

  • Hypertensive heart disease and post-myocardial-infarction heart failure (HF) are major causes of cardiovascular mortality.
  • Despite current therapies, HF incidence is rising globally.
  • Maladaptive cardiomyocyte hypertrophy, involving altered gene expression, drives HF progression.

Purpose of the Study:

  • To investigate the role of histone acetylation in maladaptive cardiomyocyte hypertrophy.
  • To explore the potential of curcumin as a therapeutic agent for HF.

Main Methods:

  • Examined the regulation of histone acetylation by histone acetyltransferase (p300) and histone deacetylase in cardiomyocytes.
  • Assessed the effect of curcumin on p300-mediated nuclear acetylation.

Main Results:

  • Excessive acetylation of cardiomyocyte nuclei is a key feature of maladaptive hypertrophy.
  • Curcumin was found to inhibit p300-mediated nuclear acetylation.

Conclusions:

  • Curcumin's inhibition of nuclear acetylation suggests its therapeutic potential for heart failure.
  • Further clinical studies are warranted to establish curcumin's efficacy and safety for HF treatment.

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