Mechanisms of disease: the oxidative stress theory of diabetic neuropathy.

Mechanisms of disease: the oxidative stress theory of diabetic neuropathy.
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DOI:
10.1007/s11154-008-9104-2
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发表时间:
2008-12
影响因子:
8.2
通讯作者:
Feldman, Eva L.
Feldman, Eva L.
中科院分区:
医学2区
文献类型:
--
作者:
Figueroa-Romero, Claudia;Sadidi, Mahdieh;Feldman, Eva L.

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糖尿病神经病变是糖尿病最常见的并发症,影响50%的糖尿病患者。目前,糖尿病神经病变的唯一治疗方法是血糖控制和仔细的足部护理。在这篇综述中,我们讨论的想法,过量的葡萄糖超载的电子传递链,导致生产超氧化物和随后的线粒体和胞质氧化应激。代谢和血管通路的缺陷与氧化应激交叉,产生糖尿病神经病变中存在的神经损伤的发作和进展。这些途径包括晚期糖基化终产物的产生,山梨醇、己糖胺和蛋白激酶C途径的改变以及聚ADP核糖聚合酶的激活。新的生物信息学方法可以增强当前的研究,并导致新的发现,以了解糖尿病神经病变的发病机制,并确定更有效的分子治疗靶点。
Diabetic neuropathy is the most common complication of diabetes, affecting 50% of diabetic patients. Currently, the only treatment for diabetic neuropathy is glucose control and careful foot care. In this review, we discuss the idea that excess glucose overloads the electron transport chain, leading to the production of superoxides and subsequent mitochondrial and cytosolic oxidative stress. Defects in metabolic and vascular pathways intersect with oxidative stress to produce the onset and progression of nerve injury present in diabetic neuropathy. These pathways include the production of advanced glycation end products, alterations in the sorbitol, hexosamine and protein kinase C pathways and activation of Poly-ADP ribose polymerase. New bioinformatics approaches can augment current research and lead to new discoveries to understand the pathogenesis of diabetic neuropathy and to identify more effective molecular therapeutic targets.
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