Nitin Tyagi*, Aroop Mohanty, Charanjeet Kaur, Ankita Kabi, Supriti Kumari, Swati Soni, Ankita Raj, Dhivya S., Veenu Rajdan, Deepak Tangadi and Bhaskar Charana Kabi


Coronary artery disease (CAD) is a common and fatal chronic disease with high mortality. It is estimated that there have been 17.5 million deaths every year worldwide, with most of the cardiovascular events having occurred below the age of 75 years. Previous studies have shown that CAD is caused by various factors, such as inflammation, gender, age, smoking, soy food intake, hypertension, and diabetes, as well as hereditary factors. The underlying pathological mechanism of CAD is atheroma plaque instability, which is characterized by chronic inflammation caused by oxidized lipids adherent on the inner layer of the arterial wall. Recent studies have shown that inflammation-related genes might be correlated with CAD risk. Interleukin-6 (IL-6) is a proinflammatory and immunoregulatory cytokine found in diverse tissues, including fibroblasts, monocytes, adipocytes, and endothelial cells. IL-6 has a role in the genesis and maintenance of the inflammatory response. The polymorphisms of the IL-6 gene are associated with different levels of secreted protein according to the genotype. Two functional variants in the IL-6 gene, -174 G>C (rs1800795) and -572 C>G (rs1800796), have been widely investigated with relation to their association with risk of various disease. These two gene polymorphisms may influence CAD susceptibility by altering gene regulation and protein expression. Several studies show that IL-6 gene polymorphisms are associated with risk for CAD, but different studies have reported conflicting results.

Keywords: CAD, IL-6 gene, Polymorphims.

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