Key result
Epigenetic modifications regulate >9,000 candidate active enhancers in failing hearts, though no FDA-approved epigenetic therapies currently prevent HFrEF or HFpEF.
This review summarizes emerging evidence that epigenetic mechanisms—including DNA methylation, chromatin remodeling, histone modifications, and microRNAs—contribute to adverse cardiac remodeling in HFrEF and HFpEF, though clinical translation of epigenetic therapies remains investigational.
Epigenetic therapies should not yet inform HFrEF or HFpEF management; leaves open whether targeting enhancers can yield approved interventions.
Chronic heart failure (HF) is a leading clinical and public problem posing a higher risk of morbidity and mortality in different populations. HF appears to be in both phenotypic forms: HF with reduced left ventricular ejection fraction (HFrEF) and HF with preserved left ventricular ejection fraction (HFpEF). Although both HF phenotypes can be distinguished through clinical features, co-morbidity status, prediction score, and treatment, the clinical outcomes in patients with HFrEF and HFpEF are similar. In this context, investigation of various molecular and cellular mechanisms leading to the development and progression of both HF phenotypes is very important. There is emerging evidence that epigenetic regulation may have a clue in the pathogenesis of HF. This review represents current available evidence regarding the implication of epigenetic modifications in the development of different HF phenotypes and perspectives of epigenetic-based therapies of HF.
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Alexander Е. Berezin (2016) conducted a review in Chronic heart failure (HFrEF and HFpEF). Epigenetic modifications and epigenetic-based therapies (DNA methyltransferase inhibitors, histone deacetylase inhibitors, microRNA regulation) was evaluated on Development and progression of heart failure phenotypes (HFrEF and HFpEF) and adverse cardiac remodeling. Epigenetic modifications regulate >9,000 candidate active enhancers in failing hearts, though no FDA-approved epigenetic therapies currently prevent HFrEF or HFpEF.
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