Review Article
Year: 2020 | Month: January-March | Volume: 5 | Issue: 1 | Pages: 32-41
Endothelial Nitric Oxide Synthase (T786C) Gene Polymorphism and Coronary Artery Disease: A Review
Namrata Bhutani, Deepak Tangadi
Senior Resident, Department Of Biochemistry, Vardhaman Mahavir Medical College, New Delhi
Corresponding Author: Deepak Tangadi
ABSTRACT
Coronary Artery Disease (CAD) is the most common type of heart disease. Globally, CAD is the leading cause of death and is predicted to remain so for the next 20 years. NO has been reported to exert various physiological roles due to its ability to induce vasodilatation. Other physiological roles of NO have been demonstrated that include its role in immune system, nervous system, inflammation and blood flow. NO has been noted to relax the smooth muscle and walls of arterioles. A common feature of many cardiovascular risk factors (including hypertension, diabetes, insulin resistance, obesity and hyperlipidemia) is endothelial dysfunction. Because the endothelium normally protects against the processes involved in atherogenesis – namely, smooth muscle cell proliferation, inflammation and thrombosis – endothelial dysfunction is an important final common pathway by which these risk factors increase atherosclerosis. This review article aims to understand the complex relationships between insulin resistance, visceral adiposity and endothelial dysfunction, the task before us is to translate this knowledge into effective treatments to reduce CVD, which is the leading cause of morbidity and mortality from diabetes and related metabolic diseases.
Keywords: Endothelial nitric oxide synthase (T-786C), gene polymorphism, Coronary artery disease, CAD.