Endothelial dysfunction and vascular inflammation in type 2 diabetes: interaction of AGE/RAGE and TNF-alpha signaling.
作者信息
Csiszar Anna, Ungvari Zoltan
出版信息
Am J Physiol Heart Circ Physiol. 2008 Aug;295(2):H475-6. doi: 10.1152/ajpheart.00644.2008. Epub 2008 Jul 3.
Abstract
摘要
相似文献
1
Endothelial dysfunction and vascular inflammation in type 2 diabetes: interaction of AGE/RAGE and TNF-alpha signaling.2型糖尿病中的内皮功能障碍与血管炎症：晚期糖基化终末产物/晚期糖基化终末产物受体（AGE/RAGE）与肿瘤坏死因子-α（TNF-α）信号通路的相互作用
Am J Physiol Heart Circ Physiol. 2008 Aug;295(2):H475-6. doi: 10.1152/ajpheart.00644.2008. Epub 2008 Jul 3.
2
AGE/RAGE produces endothelial dysfunction in coronary arterioles in type 2 diabetic mice.晚期糖基化终末产物/晚期糖基化终末产物受体在2型糖尿病小鼠的冠状动脉小动脉中导致内皮功能障碍。
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Role of MCP-1 in tumor necrosis factor-alpha-induced endothelial dysfunction in type 2 diabetic mice.单核细胞趋化蛋白-1在2型糖尿病小鼠肿瘤坏死因子-α诱导的内皮功能障碍中的作用
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Advanced glycation end products (AGEs) on the surface of diabetic erythrocytes bind to the vessel wall via a specific receptor inducing oxidant stress in the vasculature: a link between surface-associated AGEs and diabetic complications.糖尿病红细胞表面的晚期糖基化终末产物（AGEs）通过特定受体与血管壁结合，在脉管系统中诱导氧化应激：表面相关AGEs与糖尿病并发症之间的联系。
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The receptor for advanced glycation end products is induced by the glycation products themselves and tumor necrosis factor-alpha through nuclear factor-kappa B, and by 17beta-estradiol through Sp-1 in human vascular endothelial cells.晚期糖基化终产物受体在人血管内皮细胞中可被糖基化产物自身及肿瘤坏死因子-α通过核因子-κB诱导产生，也可被17β-雌二醇通过Sp-1诱导产生。
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The receptor for advanced glycation end-products has a central role in mediating the effects of advanced glycation end-products on the development of vascular disease in diabetes mellitus.晚期糖基化终产物受体在介导晚期糖基化终产物对糖尿病血管疾病发展的影响中起核心作用。
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本文引用的文献
1
AGE/RAGE produces endothelial dysfunction in coronary arterioles in type 2 diabetic mice.晚期糖基化终末产物/晚期糖基化终末产物受体在2型糖尿病小鼠的冠状动脉小动脉中导致内皮功能障碍。
Am J Physiol Heart Circ Physiol. 2008 Aug;295(2):H491-8. doi: 10.1152/ajpheart.00464.2008. Epub 2008 Jun 6.
2
Increased mitochondrial H2O2 production promotes endothelial NF-kappaB activation in aged rat arteries.线粒体过氧化氢生成增加促进老年大鼠动脉内皮细胞中核因子κB的激活。
Am J Physiol Heart Circ Physiol. 2007 Jul;293(1):H37-47. doi: 10.1152/ajpheart.01346.2006. Epub 2007 Apr 6.
3
Anti-inflammatory effects of the advanced glycation end product inhibitor LR-90 in human monocytes.晚期糖基化终产物抑制剂LR-90对人单核细胞的抗炎作用
Diabetes. 2007 Mar;56(3):647-55. doi: 10.2337/db06-0936.
4
Tumor necrosis factor-alpha induces endothelial dysfunction in Lepr(db) mice.肿瘤坏死因子-α 诱导 Lepr(db) 小鼠的内皮功能障碍。
Circulation. 2007 Jan 16;115(2):245-54. doi: 10.1161/CIRCULATIONAHA.106.650671. Epub 2007 Jan 2.
5
Vasculoprotective effects of anti-tumor necrosis factor-alpha treatment in aging.抗肿瘤坏死因子-α治疗在衰老过程中的血管保护作用。
Am J Pathol. 2007 Jan;170(1):388-98. doi: 10.2353/ajpath.2007.060708.
6
Advanced glycation end products: sparking the development of diabetic vascular injury.晚期糖基化终末产物：引发糖尿病血管损伤的发展
Circulation. 2006 Aug 8;114(6):597-605. doi: 10.1161/CIRCULATIONAHA.106.621854.
7
Tumor necrosis factor-alpha induces endothelial dysfunction in the prediabetic metabolic syndrome.肿瘤坏死因子-α在糖尿病前期代谢综合征中诱导内皮功能障碍。
Circ Res. 2006 Jul 7;99(1):69-77. doi: 10.1161/01.RES.0000229685.37402.80. Epub 2006 Jun 1.
8
Proinflammatory phenotype of coronary arteries promotes endothelial apoptosis in aging.冠状动脉的促炎表型会促进衰老过程中的内皮细胞凋亡。
Physiol Genomics. 2004 Mar 12;17(1):21-30. doi: 10.1152/physiolgenomics.00136.2003.
9
Aging-induced proinflammatory shift in cytokine expression profile in coronary arteries.衰老诱导冠状动脉中细胞因子表达谱向促炎状态转变。
FASEB J. 2003 Jun;17(9):1183-5. doi: 10.1096/fj.02-1049fje. Epub 2003 Apr 22.
10
Increased superoxide production in coronary arteries in hyperhomocysteinemia: role of tumor necrosis factor-alpha, NAD(P)H oxidase, and inducible nitric oxide synthase.高同型半胱氨酸血症患者冠状动脉中超氧化物生成增加：肿瘤坏死因子-α、NAD(P)H氧化酶和诱导型一氧化氮合酶的作用
Arterioscler Thromb Vasc Biol. 2003 Mar 1;23(3):418-24. doi: 10.1161/01.ATV.0000061735.85377.40. Epub 2003 Feb 13.
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