Lovastatin regulates hypercholesterolemia and type II diabetes via BIRC2, LDLR, APOB, CASP3, CASP6, CASP9, XIAP and APAF1 genes: A System Pharmacology approach

Abstract

Cardiovascular diseases are considered a major causative factor for the increasing rate of global mortality rate. Rendering to an approximation of the World Health Organization (WHO), 17.9 million people worldwide were affected by cardiovascular diseases. The behavioral risk factors such as tobacco use, unhealthy diet, obesity, physical inactivity, and harmful use of alcohol were found to play a significant role in the onset of cardiovascular diseases. Hypertension, diabetes, and hyperlipidemia are considered clinical factors associated with the prevalence of cardiovascular diseases. Among these clinical factors hyperlipidemia, which is characterized by increased levels of serum cholesterol, is highly related to the pathophysiological mechanism associated with cardiovascular diseases. Several medications are available for lowering abnormal serum cholesterol levels. Lovastatin, which belongs to the class of statins aids in lowering cholesterol levels by inhibiting hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase, a significant enzyme required for cholesterol biosynthesis. Lovastatin is also involved in regulating the pathogenesis of type 2 diabetes. In this study, we explored the association between Lovastatin interacting genes in Hypercholesterolemia pathways with genes associated with Type 2 Diabetes mellitus by employing systems biology approach. Our studies identified the significance of key genes such as BIRC2, LDLR, APOB, CASP3, CASP6, CASP9, XIAP, and APAF1 in the regulation of hypercholesterolemia and type 2 diabetes.