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Opinion Article - (2022)Volume 4, Issue 4
Epigenetics is a relatively new field of study that explores how gene expression is regulated by changes in DNA methylation, histone modification, and other factors that do not affect the underlying DNA sequence. Researchers are beginning to understand how epigenetic changes can influence cardiovascular health, from the development of congenital heart disease to the progression of heart failure.
During embryonic development, epigenetic changes play a critical role in shaping the formation of the heart. One study found that DNA methylation patterns differ between the left and right ventricles of the heart, suggesting that epigenetic regulation is involved in the asymmetric development of the heart. Other studies have shown that epigenetic changes can lead to abnormal heart development, resulting in congenital heart defects such as Tetralogy of Fallot or atrial septal defects.
Epigenetic changes can also be inherited from one generation to the next, which may increase the risk of cardiovascular disease. For example, studies have found that children of women who smoked during pregnancy have increased levels of DNA methylation in genes associated with cardiovascular disease, such as the ATP-Binding Cassette Transporter A1 (ABCA1) gene. Similarly, a study of families with a history of heart disease found that DNA methylation changes in the gene for endothelial Nitric Oxide Synthase (eNOS) were associated with an increased risk of coronary artery disease.
Epigenetic changes can also be influenced by environmental factors, such as diet and exercise. Studies have shown that a highfat diet can lead to epigenetic changes in genes associated with lipid metabolism and inflammation, which may contribute to the development of atherosclerosis. Similarly, exercise has been shown to induce epigenetic changes that reduce the risk of cardiovascular disease, such as increasing DNA methylation in the gene for Angiotensin Converting Enzyme (ACE), which is involved in blood pressure regulation.
Heart failure is a complex syndrome that can result from a variety of cardiovascular diseases, including coronary artery disease, hypertension, and valvular heart disease. Epigenetic changes have been implicated in the progression of heart failure, with studies showing that changes in DNA methylation, histone modification, and microRNA expression can all contribute to the development of cardiac dysfunction.
One study found that DNA methylation changes in the gene for sarcoplasmic reticulum calcium ATPase (SERCA2a), which plays a critical role in calcium homeostasis in cardiac muscle cells, were associated with decreased expression of the gene and impaired cardiac function in patients with heart failure. Similarly, a study of microRNA expression in patients with heart failure found that downregulation of miR-25, which regulates the expression of the gene for the calcium handling protein SERCA2a, was associated with impaired cardiac function and a worse prognosis..
Given the role of epigenetic changes in the development and progression of cardiovascular disease, researchers are exploring the potential of epigenetic therapies for the treatment of heart disease. One approach involves the use of small molecules that target epigenetic enzymes, such as DNA methyltransferases and histone deacetylases, to modify the epigenetic landscape of cells. Several studies have shown that these small molecule inhibitors can reduce the progression of atherosclerosis and improve cardiac function in animal models of heart disease. Clinical trials are now underway to test the safety and efficacy of these epigenetic therapies in humans..
Citation: Idris R (2022) Cardiovascular Epigenetics: Understanding the Role of Gene Expression in Heart Health. J Epigenetics Res 4: 121.
Received: 29-Nov-2022, Manuscript No. EROA-22-23538; Editor assigned: 01-Dec-2022, Pre QC No. EROA-22-23538 (PQ); Reviewed: 15-Dec-2022, QC No. EROA-22-23538; Revised: 22-Dec-2022, Manuscript No. EROA-22-23538 (R); Published: 29-Dec-2022 , DOI: 10.35248/EROA.22.4.121
Copyright: © 2022 Idris R. This is an open access article distributed under the term of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.