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[蛋白质糖基化与内皮功能障碍]

[Protein glycation and endothelium dysfunction].

作者信息

Grossin Nicolas, Wautier Jean-Luc

机构信息

Laboratoire de Biologie Vasculaire et Cellulaire, Institut National Transfusion Sanguine, Paris.

出版信息

J Soc Biol. 2007;201(2):175-84. doi: 10.1051/jbio:2007022.

DOI:10.1051/jbio:2007022
PMID:17978751
Abstract

Advanced glycation end-products (AGE) are a group of heterogeneous molecules found in higher levels during diabetes, end stage renal failure and aging. Vascular alteration is correlated with their accumulation as during retinopathy or glomerulosclerosis. Glycation of extracellular matrix proteins is associated with diabetic angiopathy. AGE stimulate endothelial cell via the interaction with the receptor RAGE, leading to an inflammatory state with increased adhesion molecule expression, chemoattractant factor and tissue factor production. RAGE activation by AGE triggers reactive oxygen species production by NADPH oxydase. Agents that inhibit AGE formation, stimulate their degradation or neutralize their binding to RAGE represent new approaches to limit the deleterious activities of AGE.

摘要

晚期糖基化终末产物(AGE)是一组异质性分子,在糖尿病、终末期肾衰竭和衰老过程中含量较高。血管改变与它们的积累相关,如在视网膜病变或肾小球硬化过程中。细胞外基质蛋白的糖基化与糖尿病性血管病变有关。AGE通过与受体RAGE相互作用刺激内皮细胞,导致炎症状态,增加黏附分子表达、趋化因子和组织因子生成。AGE激活RAGE会触发NADPH氧化酶产生活性氧。抑制AGE形成、促进其降解或中和其与RAGE结合的药物是限制AGE有害活性的新方法。

相似文献

1
[Protein glycation and endothelium dysfunction].[蛋白质糖基化与内皮功能障碍]
J Soc Biol. 2007;201(2):175-84. doi: 10.1051/jbio:2007022.
2
Protein glycation: a firm link to endothelial cell dysfunction.蛋白质糖基化:与内皮细胞功能障碍的紧密联系。
Circ Res. 2004 Aug 6;95(3):233-8. doi: 10.1161/01.RES.0000137876.28454.64.
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Advanced glycation end-products and atherosclerosis.晚期糖基化终末产物与动脉粥样硬化
Ann Med. 1996 Oct;28(5):419-26. doi: 10.3109/07853899608999102.
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Advanced glycation end products activate endothelium through signal-transduction receptor RAGE: a mechanism for amplification of inflammatory responses.晚期糖基化终末产物通过信号转导受体RAGE激活内皮细胞:一种炎症反应放大机制。
Circulation. 2002 Feb 19;105(7):816-22. doi: 10.1161/hc0702.104183.
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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。
Proc Natl Acad Sci U S A. 1994 Aug 2;91(16):7742-6. doi: 10.1073/pnas.91.16.7742.
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Activation of receptor for advanced glycation end products: a mechanism for chronic vascular dysfunction in diabetic vasculopathy and atherosclerosis.晚期糖基化终末产物受体的激活:糖尿病血管病变和动脉粥样硬化中慢性血管功能障碍的一种机制。
Circ Res. 1999 Mar 19;84(5):489-97. doi: 10.1161/01.res.84.5.489.
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[Advanced glycation end products: A risk factor for human health].[晚期糖基化终末产物:人类健康的一个风险因素]
Ann Pharm Fr. 2014 Nov;72(6):400-8. doi: 10.1016/j.pharma.2014.05.002. Epub 2014 Jun 18.
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Diabetes and advanced glycation endproducts.糖尿病与晚期糖基化终末产物
J Intern Med. 2002 Feb;251(2):87-101. doi: 10.1046/j.1365-2796.2002.00932.x.
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Activation of NADPH oxidase by AGE links oxidant stress to altered gene expression via RAGE.晚期糖基化终末产物激活NADPH氧化酶,通过晚期糖基化终末产物受体将氧化应激与基因表达改变联系起来。
Am J Physiol Endocrinol Metab. 2001 May;280(5):E685-94. doi: 10.1152/ajpendo.2001.280.5.E685.
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[Non-enzymatic glycation and oxidative stress in chronic illnesses and diabetes mellitus].慢性病与糖尿病中的非酶糖基化和氧化应激
Med Klin (Munich). 1999 Jan 15;94(1):29-38. doi: 10.1007/BF03044692.

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Hyperglycemic oxoaldehyde, glyoxal, causes barrier dysfunction, cytoskeletal alterations, and inhibition of angiogenesis in vascular endothelial cells: aminoguanidine protection.高血糖醛,即乙二醛,可导致血管内皮细胞的屏障功能障碍、细胞骨架改变和血管生成抑制:氨基胍的保护作用。
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