Type 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.

中文翻译：

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氧化应激相关遗传变异的影响：“阐明活性氧影响抗氧化基因多态性的作用”，2 型糖尿病相关肾病的风险分层：系统评价

2 型糖尿病被认为与微血管并发症有关，包括糖尿病视网膜病变、肾病和神经病变。氧化应激在 DN 的发病机制中起主导作用，还影响代谢活动及其血流动力学途径，与肾脏并发症具有多种关联，其中之一是糖尿病肾病，它是终末期肾病的重要原因。DN 的肾损伤主要与氧化应激有关，影响代谢活动及其血流动力学途径。高血糖是糖尿病的一个标志性特征，它会促进糖尿病患者的病情，导致更高的活性氧产生，最终导致氧化应激增加，这被认为是引发糖尿病肾病的重要事件。与氧化应激相关，ROS主要由多种重要途径产生，这为抗氧化治疗方法预防DN肾小管损伤的发生和进展/加重铺平了道路。最重要的抗氧化酶包括超氧化物歧化酶、过氧化氢酶、谷胱甘肽-S-转移酶和谷胱甘肽过氧化物酶，被认为是参与反应性代谢物组装和排出的主要元素。因此，本综述强调抗氧化基因多态性也推测这些抗氧化基因中的多态性可能是DN发病的主要原因。因此，它也可以回答研究人员提出的许多问题，临床医生检测这些抗氧化基因的单核苷酸多态性并采取靶向治疗方法可以增强遗传变化，有助于减轻 DN 早期的严重程度。此外，该文献综述还表明了区域人群研究检测抗氧化基因SNP的重要性，这反过来又反映了与T2D相关的DN发病机制中氧化应激的状态。