首页> 外文期刊>Proceedings of the Romanian Academy, Series B. Chemistry, life sciences and geosciences >OXIDATIVE STRESS CONTRIBUTIONS TO CHRONIC COMPLICATIONSIN DIABETES
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OXIDATIVE STRESS CONTRIBUTIONS TO CHRONIC COMPLICATIONSIN DIABETES

机译:糖尿病对慢性并发症的氧化应激贡献。

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摘要

Diabetes Mellitus is a serious global health problem. Both type 1 and type 2 diabetes markedlyincrease the risk of microvascular and macrovascular complications. Chronic complications ofdiabetes (retinopathy, nephropathy, neuropathy, and diabetes accelerated arteriosclerosis) represent amajor medical and economical concern. Several pathogenic mechanisms were proposed to beresponsible for the development of long-term complications of diabetes (i.e. increase polyol pathwayflux, increased advanced glycation end products, activation of proteinkinase C, increased hexosaminepathway flux). A coherent pathogenic mechanism has just recently evolved by the discovery that eachof the mechanisms mentioned reflects a single hyperglycemia-induced process: overproduction ofreactive oxygen species by the mitochondria electron-transport chain. Oxidative stress is defined astissue injury resulting from a disturbance in the equilibrium between the production free radicals andantioxidant defense mechanisms. In this review, we consider how glucose-induced oxidative stressmay lead to microvascular and cardiovascular complications.
机译:糖尿病是一个严重的全球性健康问题。 1型和2型糖尿病都显着增加了微血管和大血管并发症的风险。糖尿病的慢性并发症(视网膜病,肾病,神经病和糖尿病加速的动脉硬化)代表了医学和经济上的重大关注。提出了几种致病机制来应对糖尿病的长期并发症(即增加多元醇途径通量,增加晚期糖基化终产物,激活蛋白激酶C,增加己糖胺途径通量)。通过发现以下提到的每种机制反映了单个高血糖诱导的过程,最近才发展出一种连贯的致病机制:通过线粒体电子传输链过量生产活性氧。氧化应激是指由于自由基产生和抗氧化防御机制之间的平衡失调而引起的星形线损伤。在这篇综述中,我们考虑了葡萄糖诱导的氧化应激如何导致微血管和心血管并发症。

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