Abstract
AbstractType 2 diabetes mellitus is believed to be associated with microvascular complications which include diabetic retinopathy, nephropathy, and neuropathy. Oxidative stress plays a predominant role in the pathogenesis of DN and also influences metabolic endeavor and its hemodynamic pathways to possess various associations with renal complications, and one such is diabetic nephropathy which is the insignificant cause of end-stage renal disease. Renal injury in DN is predominantly related to the inclined oxidative stress, with influential metabolic endeavor and its hemodynamic pathways. Hyperglycemia, an hallmark feature of diabetes, promotes conditions of the diabetic patients responsible for higher reactive oxygen species production, which ultimately leads to increased oxidative stress, and this is considered to be the important event in the initiation of DN. Pertaining to oxidative stress, ROS is generated mostly by the variety of important pathways, in which this paves the way for antioxidant therapeutic approach preventing the initiation and progression/aggravation of tubular injury in DN. The most salient antioxidant enzymes including superoxide dismutase, catalase, glutathione-S-transferase, and glutathione peroxidase are considered as prime elements involved in the assembly and discharge of reactive metabolites. Therefore, this review highlights that antioxidant gene polymorphisms also postulate that this in these antioxidant genes may be a major cause for the pathogenesis of DN. Hence, it could also answer many questions put forth by researchers, and clinicians detecting the single-nucleotide polymorphism of these antioxidant genes and targeting therapeutic approach can enhance the genetic changes and help to reduce severity at the early stages of DN. Additionally, this literature review also shows the importance of regional population studies on detecting the SNPs of antioxidant gene which in turn reflects the status of oxidative stress involved in the pathogenesis of DN associated with T2D.
Publisher
Springer Science and Business Media LLC
Cited by
1 articles.
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