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糖尿病并发症统一机制学说与糖尿病视网膜病变 被引量:5

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摘要 糖尿病并发症的发病机制一直是人们研究的焦点之一。1966年,Gabbay等提出了多元醇通路及其活性增强在糖尿病周围神经病变发病中作用,首次揭示了糖尿病并发症的分子机制。随后,人们相继发现了非酶糖基化终产物(AGE)增加、蛋白激酶C(PKC)活性增强及氨基己糖通路增加与糖尿病并发症发病有关。但是,临床上对这些通路分别予以抑制却未取得预期的试验结果。
作者 郑志 许迅
出处 《中华医学杂志》 CAS CSCD 北大核心 2007年第28期2011-2013,共3页 National Medical Journal of China
基金 上海市领军人才培养计划基金(2005-0110)
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同被引文献59

  • 1李鹏,马效工,安晓.糖尿病性角膜上皮病变机制研究现状[J].国际眼科杂志,2005,5(1):150-154. 被引量:7
  • 2邹海东,张皙,朱剑锋,汪枫桦,许迅,王伟伟,吴美芳.上海市北新泾街道糖尿病患者视网膜病变的患病率调查[J].中华眼底病杂志,2006,22(1):31-34. 被引量:82
  • 3陈红霞,张喆.糖尿病周围神经病变的病理生理机制研究进展[J].国际内分泌代谢杂志,2007,27(B04):47-49. 被引量:21
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