Advanced glycation end products, oxidative stress and diabetic nephropathy
Advanced glycation end products, oxidative stress and diabetic nephropathy
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DOI：
10.4161/oxim.3.2.4
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发表时间：
2010-03
影响因子：
--
通讯作者：
S. Yamagishi;T. Matsui
中科院分区：
文献类型：
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作者：
S. Yamagishi;T. Matsui
2007年，全球约有2.46亿人患有糖尿病。预计到2030年，全球糖尿病患者人数将增加到3.7亿。随着糖尿病的患病率在世界范围内上升到流行病的比例，糖尿病肾病已成为最具挑战性的健康问题之一。严格控制血糖和血压等治疗方案对于预防糖尿病肾病是有效的，但还远不能令人满意，而且患有终末期肾病的糖尿病患者数量仍在增加。因此，应该开发一种新的治疗策略，可以阻止糖尿病肾病的进展。越来越多的证据表明，晚期糖基化终产物（AGEs），衰老的大蛋白衍生物在糖尿病下以加速的速率形成，通过氧化应激的产生在糖尿病肾病中发挥作用。本文就AGEs及其受体-氧化应激系统在糖尿病肾病中的病理生理作用作一综述。
About 246 million people worldwide had diabetes in 2007. The global figure of people with diabetes is projected to increase to 370 million in 2030. As the prevalence of diabetes has risen to epidemic proportions worldwide, diabetic nephropathy has become one of the most challenging health problems. Therapeutic options such as strict blood glucose and blood pressure controls are effective for preventing diabetic nephropathy, but are far from satisfactory, and the number of diabetic patients on end-stage renal disease is still increasing. Therefore, a novel therapeutic strategy that could halt the progression of diabetic nephropathy should be developed. There is accumulating evidence that advanced glycation end products (AGEs), senescent macroprotein derivatives formed at an accelerated rate under diabetes, play a role in diabetic nephropathy via oxidative stress generation. In this paper, we review the pathophysiological role of AGEs and their receptor (RAGE)-oxidative stress system in diabetic nephropathy.