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防治糖尿病并发症的新思路——干预过氧化物产生过量 被引量:3

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摘要 在高血糖致血管损伤的过程中,线粒体电子传递链过氧化物产生过量是晚期糖基化终末产物形成、蛋白激酶C激活、多元醇通路和氨基己糖通路活性增高的共同机制。阻止过氧化物的生成或干预其作用将是糖尿病并发症防治的重要方向,其中转酮醇酶激活剂、多(ADP-核糖)聚合酶抑制剂和各种新型抗氧化剂备受关注。
出处 《国外医学(内分泌学分册)》 2005年第6期391-393,共3页 Foreign Medical Sciences(Section of Endocrinology)
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  • 1Brownlee M. The pathobiology of diabetic complications: a unifying mechanism. Diabetes, 2005,54:1615-1625. 被引量:1
  • 2He Z, King GL. Microvascular complications of diabetes. Endocrinol Metab Clin North Am,2004,33:215-238. 被引量:1
  • 3Jakus V, Rietbrock N. Advanced glycation end-products and the progress of diabetic vascular complications. Physiol Res, 2004,53:131 - 142. 被引量:1
  • 4Brownlee M. Biochemistry and molecular cell biology of diabetic complications. Nature, 2001,414:813-820. 被引量:1
  • 5Evans JL, Goldfine ID, Maddux BA, et al. Oxidative stress and stress-activated signaling pathways: a unifying hypothesis of type 2 diabetes. Endocr Rev, 2002,23: 599-622. 被引量:1
  • 6Nishikawa T, Edelstein D, Du X, et al. Normalizing mitochondrial superoxide production blocks three pathways of hyperglycaemic damage. Nature, 2000,404: 787-790. 被引量:1
  • 7Green K, Brand MD, Murphy MP. Prevention of mitochondrial oxidative damage as a therapeutic strategy in diabetes. Diabetes, 2004, 53: S110-S118. 被引量:1
  • 8Du X,Matsumura T, Edelstein D,et al. Inhibition of GAPDH activity by poly(ADP-ribose) polymerase activates three major pathways of hyperglycemic damage in endothelial cells. J Clin Invest, 2003, 112: 1049-1057. 被引量:1
  • 9Soriano FG, Virag L, Szabo C. Diabetic endothelial dysfunction: role of reactive oxygen and nitrogen species production and poly(ADP-ribose)polymerase activation. J Mol Med,2001,79:437-448. 被引量:1
  • 10Sheetz MJ, King GL. Molecular understanding of hyperglycemia's adverse effects for diabetic complications. JAMA, 2002,288: 2579-2588. 被引量:1

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