Abstract
In recent decades, oxidative stress has become a focus of interest in most biomedical disciplines and many types of clinical research. Increasing evidence shows that oxidative stress is associated with the pathogenesis of diabetes, obesity, cancer, ageing, inflammation, neurodegenerative disorders, hypertension, apoptosis, cardiovascular diseases, and heart failure. Based on these studies, an emerging concept is that oxidative stress is the “final common pathway” through which the risk factors for several diseases exert their deleterious effects. Oxidative stress causes a complex dysregulation of cell metabolism and cell–cell homeostasis; in particular, oxidative stress plays a key role in the pathogenesis of insulin resistance and β-cell dysfunction. These are the two most relevant mechanisms in the pathophysiology of type 2 diabetes and its vascular complications, the leading cause of death in diabetic patients.
Highlights
The biological systems living in aerobic conditions are exposed to oxidants, either generated intentionally or as byproducts
Activation of the polyol pathway can contribute to oxidative stress, by causing nicotinamide adenine dinucleotide phosphate (NADPH) depletion and consequent decrease in intracellular glutathione. Another factor involved in diabetic neuropathy is increased DNA damage stemming from enhanced production of nitric oxide (NO); the resulting activation of poly ADP ribose polymerase (PARP) lowers NADPH and is a stimulus for secretion of inflammatory mediators [146]
A large body of evidence suggests that oxidative stress has a key role in the pathogenesis of diabetes and its complications
Summary
The biological systems living in aerobic conditions are exposed to oxidants, either generated intentionally or as byproducts. These oxidants occur in two categories consisting of paramagnetic free radicals: reactive oxygen species (ROS) and reactive nitrogen species (RNS). ROS and RNS, previously considered to be toxic agents capable to damage molecules, have critical biological functions essential for normal physiology. All these species are able to initiate or mediate many enzyme- and gene-dependent reactions in both physiological and pathophysiological processes. It is widely believed that multiple pathogenic mechanisms involve disequilibrium in the redox balance as the final common pathway [1]
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