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Histone Lactylation Promotes Pressure Overload-Induced Cardiac Hypertrophy and Heart Failure by Regulating TGFB2

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Histone lactylation, a marker of increased glycolysis, promotes cardiac hypertrophy and heart failure. Inhibiting this epigenetic modification may offer a new therapeutic strategy for heart disease.

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Area of Science:

  • Epigenetics
  • Cardiovascular Biology
  • Metabolic Regulation

Background:

  • Cardiac hypertrophy involves metabolic changes, including enhanced glycolysis.
  • Histone lactylation, linked to glycolysis, regulates gene transcription but its role in cardiac hypertrophy is unknown.

Purpose of the Study:

  • To investigate the role of histone lactylation in pathological cardiac hypertrophy.
  • To identify the molecular mechanisms by which histone lactylation influences cardiac remodeling.

Main Methods:

  • Assessed histone lactylation in human and mouse hearts with hypertrophy.
  • Utilized mouse models of cardiac hypertrophy with pharmacological or genetic modulation of histone lactylation.
  • Employed in vitro cardiomyocyte models to study lactylation inhibition.
  • Identified lactylation transferases and analyzed promoter-specific lactylation.
  • Investigated the role of TGFB2 and PI3K/AKT/mTOR signaling.

Main Results:

  • Histone lactylation was elevated in failing hearts and promoted hypertrophy, fibrosis, and cardiac dysfunction.
  • Lactylation inhibition attenuated cardiac remodeling in vivo and in vitro.
  • P300 and GCN5 were identified as lactylation transferases.
  • Histone lactylation at the TGFB2 promoter increased its expression, driving hypertrophy via PI3K/AKT/mTOR signaling.

Conclusions:

  • Histone lactylation drives pathological cardiac hypertrophy and heart failure.
  • Upregulation of TGFB2 and activation of PI3K/AKT/mTOR signaling mediate these effects.
  • Histone lactylation represents an epigenetic link between metabolic reprogramming and hypertrophic signaling, offering a potential therapeutic target.