Author + information
- Received February 26, 2019
- Revision received May 29, 2019
- Accepted May 30, 2019
- Published online December 23, 2019.
- aDepartment of Cardiovascular and Metabolic Sciences, Lerner Research Institute, Cleveland Clinic, Cleveland, Ohio
- bDepartment of Cardiovascular Medicine, Heart and Vascular Institute, Cleveland Clinic, Cleveland, Ohio
- ↵∗Address for correspondence:
Dr. W.H. Wilson Tang, Department of Cardiovascular Medicine, Heart and Vascular Institute, Cleveland Clinic, 9500 Euclid Avenue, Desk J3-4, Cleveland, Ohio 44195.
• Epigenetic mechanisms associated with the pathological process of cardiac hypertrophy and failure include DNA methylation, post-modification of histones, ATP-dependent chromatin conformation and remodeling, and non-coding RNAs.
• Systemic- and cardiac-epigenetic mechanisms may both influence the disease processes of cardiac hypertrophy and failure.
• Identifying vital epigenetic machinery in cardiac diseases may facilitate developing personalized therapy for HF.
Heart failure (HF) is a complex syndrome affecting millions of people around the world. Over the past decade, the therapeutic potential of targeting epigenetic regulators in HF has been discussed extensively. Recent advances in next-generation sequencing techniques have contributed substantial progress in our understanding of the role of DNA methylation, post-translational modifications of histones, adenosine triphosphate (ATP)-dependent chromatin conformation and remodeling, and non-coding RNAs in HF pathophysiology. In this review, we summarize epigenomic studies on human and animal models in HF.
Dr. Tang is supported by grants from the National Institutes of Health (NIH) and the Office of Dietary Supplements (R01DK106000, R01HL126827), Collins Family Fund, and Wortzman Family Fund. The content is solely the responsibility of the authors and does not necessarily represent the official views of the NIH. Dr. Tang has a financial relationship with Sequana Medical Inc. and MyoKardis Inc. Dr. Liu has reported that she does not have any relationships relevant to the contents of this paper to disclose.
The authors attest they are in compliance with human studies committees and animal welfare regulations of the authors’ institutions and Food and Drug Administration guidelines, including patient consent where appropriate. For more information, visit the JACC: Basic to Translational Science author instructions page.
- Received February 26, 2019.
- Revision received May 29, 2019.
- Accepted May 30, 2019.
- 2019 The Authors
- Central Illustration
- DNA Methylation: A Potential Biomarker for HF
- Post-Translational Modifications of Histones: Dynamic Processes Accomplished by Writers and Readers Enzymatically
- ATP-Dependent Chromatin Conformation, Remodeling, and HF
- Long Non-Coding RNAs: The New Players in Epigenetic Regulation for HF
- Nutrition, Gut Microbiome, and Epigenetics: Interplay Among Host, Gut Microbiotial Metabolites, and Host Chromatin
- Therapeutic Potential of Targeting Epigenetic Regulators in HF
- Conclusions and Future Perspectives