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氧化应激与糖尿病肾病。

Oxidative stress and diabetic kidney disease.

机构信息

Harvard Medical School, Joslin Diabetes Center, One Joslin Place, Boston, MA 02215, USA.

出版信息

Curr Diab Rep. 2011 Aug;11(4):330-6. doi: 10.1007/s11892-011-0196-9.

DOI:10.1007/s11892-011-0196-9
PMID:21557044
Abstract

The number of people with diabetic kidney disease continues to increase worldwide despite current treatments. Of the pathophysiologic mechanisms that have been identified in the development and progression of diabetic nephropathy, oxidative stress (more accurately described as increased levels of reactive oxygen species; ROS) is of major importance. The increase in ROS is due to both increased production and to decreased and/or inadequate antioxidant function. To date, human clinical trials with antioxidants have not been shown to be effective. This is likely due, at least in part, to the lack of specificity of current agents. Recent research has determined both major sources of high glucose-induced cellular ROS production as well as high glucose-induced changes in antioxidant function. Treatments targeted at one or more of the specific diabetes-induced alterations in the regulation of ROS levels will likely lead to effective treatments that prevent the development and progression of diabetic kidney disease.

摘要

尽管目前已有治疗方法,但全球范围内患有糖尿病肾病的人数仍在持续增加。在糖尿病肾病的发生和发展中已确定的病理生理机制中,氧化应激(更准确地描述为活性氧增加;ROS)非常重要。ROS 的增加既归因于其产生的增加,也归因于其减少和/或功能不足。迄今为止,用抗氧化剂进行的人体临床试验并未显示出有效。这可能至少部分归因于当前药物缺乏特异性。最近的研究确定了高葡萄糖诱导的细胞 ROS 产生的主要来源,以及高葡萄糖诱导的抗氧化功能变化。针对一个或多个特定的糖尿病诱导的 ROS 水平调节改变进行治疗,可能会带来有效的治疗方法,从而预防糖尿病肾病的发生和发展。

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