Abstract
Coronary artery disease (CAD) remains the leading global public health burden in cardiovascular diseases. Atherosclerosis is a primary mechanism to cause CAD with the contribution of epidemiological, traditional, genetic, and epigenetic risk factors. Statins, prescribed drugs for lowering of cholesterol levels, also have pleiotropic effect on oxidative stress, inflammation, apoptosis, etc. Reactive oxygen species (ROS)-induced oxidative stress associates with risk factors and participates in initiation and progression of disease. ROS molecules generated as superoxides (O2•ˉ), singlet/triplet oxygen, peroxides (H2O2, ONOO−), and hydroxyl radicals (HO•) via reactions catalyzed by endothelial nitric oxide synthase, myeloperoxidase, NADPH oxidase, and xanthine oxidase enzyme are encoded by eNOS, MPO, NOX, and XO genes, respectively. Polymorphisms in eNOS, MPO, NOX, and XO genes influence the expression and attributes to interindividual variation in response to statin drugs. Differential response to statin drug insights into emerging of pharmacogenetic studies to understand the genetic makeup and treat the patient with suitable drug and dose. In clinical practice, pharmacogenetic approach toward oxidative stress is a future emerging trend in personalized medicine development.
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Acknowledgments
This work was supported by UGC, New Delhi, India: MRP-2013 (F.No.42-52/2013[SR]), BSR-Fellowship, CPEPA, and OU-DST-PURSE-II Programme (C-DST-PURSE- II/23/2017), ICMR-SRF (ID No. 2019-4183).
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Shyamala, N., Hanumanth, S.R. (2019). Pharmacogenetic Implications of Statin Therapy on Oxidative Stress in Coronary Artery Disease. In: Chakraborti, S., Dhalla, N., Dikshit, M., Ganguly, N. (eds) Modulation of Oxidative Stress in Heart Disease. Springer, Singapore. https://doi.org/10.1007/978-981-13-8946-7_26
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