کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
2773043 | 1567896 | 2016 | 7 صفحه PDF | دانلود رایگان |

• The causes of heart failure development with presentation of preserved or reduced ejection fraction are not clear
• The epigenetic modifications are discussed as a phenotypic regulator in the failing heart.
• The phenotypic response in heart failure may regulate by microRNAs via interaction with histone modification or DNA methylation.
• The epigenetic modifications of cardiomyocytes may be a target for personalized management in HF individuals.
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.
Journal: BBA Clinical - Volume 6, December 2016, Pages 31–37