Panigrahy Suchitra Kumari, Bhatt Renu, Kumar Awanish
a Department of Biotechnology , Guru Ghasidas Vishwavidyalaya (a Central University) , Bilaspur , India.
b Department of Biotechnology , National Institute of Technology (NIT) , Raipur , India.
J Drug Target. 2017 Feb;25(2):93-101. doi: 10.1080/1061186X.2016.1207650. Epub 2016 Jul 19.
Oxidative stress has been considered as a central mediator in the progression of diabetic complication. The intracellular reactive oxygen species (ROS) leads to oxidative stress and it is raised from the mitochondria as well as by activation of five major pathways: increased polyol pathway flux, activation of protein kinase C (PKC) pathway, increased formation of advanced glycation end products (AGEs), over activity of hexosamine pathway and increased production of angiotensin II. The increased ROS through these pathways leads to β-cell dysfunction and insulin resistance, responsible for cell damage and death. This review not only highlights the sources of ROS production and their involvement in the progression of diabetes, but also emphasizes on pharmacological interventions and targeting of ROS in type 2 diabetes. This review summarizes the ROS as potential therapeutic targets, based on a putative mechanism in the progression of the diabetes. It also summarizes current knowledge of ROS activation in type 2 diabetes as well as ROS as a possible target for its treatment. Eventually, it would be a promising target for various strategies and drugs to modulate ROS levels in diabetes.
氧化应激被认为是糖尿病并发症进展的核心介质。细胞内活性氧（ROS）会导致氧化应激，其产生于线粒体以及通过五条主要途径的激活：多元醇途径通量增加、蛋白激酶C（PKC）途径激活、晚期糖基化终产物（AGEs）形成增加、己糖胺途径活性过高以及血管紧张素II产生增加。通过这些途径增加的ROS会导致β细胞功能障碍和胰岛素抵抗，进而造成细胞损伤和死亡。本综述不仅强调了ROS产生的来源及其在糖尿病进展中的作用，还着重探讨了2型糖尿病中针对ROS的药物干预措施。基于糖尿病进展中的一种假定机制，本综述总结了ROS作为潜在治疗靶点的情况。它还总结了2型糖尿病中ROS激活的现有知识以及ROS作为其治疗的可能靶点。最终，调节糖尿病中ROS水平将成为各种策略和药物的一个有前景的靶点。
