Author + information
- Received June 11, 2019
- Accepted July 15, 2019
- Published online September 2, 2019.
- Barbara Rizzacasa, PhDa,
- Francesca Amati, PhDa,b,
- Francesco Romeo, MDc,d,
- Giuseppe Novelli, PhDa,e,f and
- Jawahar L. Mehta, MD, PhDf,∗ (, )@uamshealth
- aDepartment of Biomedicine and Prevention, University of Rome Tor Vergata, Rome, Italy
- bDepartment of Human Sciences and Quality of Life Promotion, University San Raffaele, Rome, Italy
- cComplex Operative Unit of Cardiology, Policlinico Tor Vergata, Rome, Italy
- dDepartment of System Medicine, University of Rome Tor Vergata, Rome, Italy
- eNeuromed IRCCS, Pozzilli, Italy
- fCentral Arkansas Veterans Healthcare System and the University of Arkansas for Medical Sciences, Little Rock, Arkansas
- ↵∗Address for correspondence:
Dr. Jawahar L. Mehta, University of Arkansas for Medical Sciences, Division of Cardiology, 4301 W Markham, Little Rock, Arkansas 72205.
• Epigenetic modifications that contribute to coronary atherosclerosis are links between genetics and the environment in CAD development.
• Results of studies conducted thus far have been rather inconsistent.
• These inconsistencies in the epigenetic field highlight the need for further research.
Coronary artery disease (CAD) and its major complication, acute myocardial infarction (AMI), are the leading causes of disability and death worldwide. An individual’s risk of developing CAD and MI is modulated by an interplay between genetic and lifestyle factors. It is now clear that epigenetics may play a central role in the development of CAD because epigenetic patterns are affected by the environment and can modulate gene expression. Here, the authors discuss the major epigenetic changes that contribute to CAD and the latest discoveries on the influence of the environment on epigenetic profiles in the development of CAD.
These studies were supported in part by the Veterans Health Administration, Office of Research and Development, Biomedical Laboratory Research and Development (grant #BX000282-09A2 to Dr. Mehta); Fondazione Roma (Sn. NCDS-2013-00000333 to Drs. Novelli and Romeo); and Bandi Ateneo “Consolidate Foundations” (AmiRNA E82F16000570005 to Dr. Amati). Dr. Mehta has served as consultant to and received grant support from Bayer, Boehringer Ingelheim, AstraZeneca, MedImmmune, and Pfizer. All other authors have reported that they have no relationships relevant to the contents of this paper to disclose.
Listen to this manuscript's audio summary by Editor-in-Chief Dr. Valentin Fuster on JACC.org.
- Received June 11, 2019.
- Accepted July 15, 2019.
- 2019 American College of Cardiology Foundation
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