Key result
Histone methylation regulates cardiac remodeling and metabolism, making its enzymes promising heart failure targets.
This review highlights the critical role of dynamic histone methylation in heart failure progression and identifies epigenetic modifying enzymes as promising therapeutic targets for future preclinical and clinical translation.
Should not yet change HF practice; extends rationale for preclinical targeting of histone methylation enzymes.
Heart failure (HF) represents the terminal stage of various cardiovascular diseases, and its prevalence continues to rise while current therapeutic approaches remain insufficient to reverse disease progression. Epigenetic regulation, with a particular focus on histone methylation, has gained increasing attention for its involvement in the initiation and advancement of HF. Histone methylation is a reversible post-translational modification controlled by histone methyltransferases and demethylases, and it participates in essential biological processes such as gene expression regulation, cell cycle, apoptosis, and metabolic reprogramming. This review systematically summarizes the multifaceted roles of histone methylation in HF, including the specific functions in cardiac regeneration, hypertrophy, fibrosis, apoptosis, metabolic remodeling, and inflammation. The review also highlights the promising effects of inhibitors that target histone methylation enzymes in animal studies, including anti-hypertrophic, anti-fibrotic, and cardioprotective properties, suggesting significant potential for clinical translation.
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Zhou et al. (2026) conducted a review in Heart Failure. Histone methylation modulators was evaluated. Histone methylation regulates cardiac regeneration, hypertrophy, fibrosis, apoptosis, and metabolism, making histone methylation enzymes promising therapeutic targets for heart failure.
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