Role of oxidative stress in the pathophysiology of type 2 diabetes and cardiovascular diseases

Abstract

Many of the cell components like mitochondria, as well as other cytosolic components, are central to and has pivotal significance in reactive oxygen species (ROS) production. A state of imbalance between ROS production and antioxidant defense mechanisms, in which ROS are favored, is termed oxidative stress. Oxidative stress is a common denominator in the progression of several deteriorating ailments, for instance, diabetes mellitus (DM) and cardiovascular diseases (CVDs). DM is a worldwide health burden, affecting people globally, and it is one of the main causative factors for death and a main risk factor for CVDs. The most prevalent type of DM is type 2 diabetes (T2D), which is a derangement of metabolism with a peculiar feature of insulin resistance and hyperglycemia. Oxidative stress promotes “overload of glucose, oxidative phosphorylation influx of polyol pathway, elevated advanced glycation products (AGEs), formation and expression at receptors site, activation of protein kinase C isoforms, and hexosamine pathway initiation.” CVDs are complex in nature with multifaceted mechanisms regarding its pathophysiology. CVDs refers to conditions that involve blocked heart and/or blood vessels resulting to diseases such as coronary heart diseases, ischemic heart diseases, atherosclerosis, stroke with hypertension, hypercholesterolemia, and/or dyslipidemia as major risk factors. We examine in this chapter the association of oxidative stress with hyperglycemia, insulin resistance, hyperinsulinemia, hypertension, hypercholesterolemia, and/or dyslipidemia, to mention a few factors in the pathogenesis of T2D and CVDs. These metabolic processes or enzymes implicated in type 2 diabetes and cardiovascular diseases are current therapeutic targets and could be explored for future/novel drug design.