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RAGE 生物学、动脉粥样硬化和糖尿病。

RAGE biology, atherosclerosis and diabetes.

机构信息

Clinical Department of Endocrinology, Diabetes and Metabolic Diseases, University Medical Centre Ljubljana, Zaloska 7, Ljubljana, Slovenia.

出版信息

Clin Sci (Lond). 2011 Jul;121(2):43-55. doi: 10.1042/CS20100501.

Abstract

Diabetes is characterized by accelerated atherosclerosis with widely distributed vascular lesions. An important mechanism by which hyperglycaemia contributes to vascular injury is through the extensive intracellular and extracellular formation of AGEs (advanced glycation end products). AGEs represent a heterogeneous group of proteins, lipids and nucleic acids, irreversibly cross-linked with reducing sugars. AGEs are implicated in the atherosclerotic process, either directly or via receptor-mediated mechanisms, the most extensively studied receptor being RAGE (receptor for AGEs). The AGE-RAGE interaction alters cellular signalling, promotes gene expression and enhances the release of pro-inflammatory molecules. It elicits the generation of oxidative stress in numerous cell types. The importance of the AGE-RAGE interaction and downstream pathways leading to injurious effects as a result of chronic hyperglycaemia in the development, progression and instability of diabetic atherosclerotic lesions has been amply demonstrated in animal studies. Moreover, the deleterious link of AGEs with diabetic vascular complications has been suggested in many human studies. In the present review, our current understanding of their role as an important mediator of vascular injury through the various stages of atherosclerosis in diabetes will be reviewed and critically assessed.

摘要

糖尿病的特征是动脉粥样硬化加速,血管病变广泛分布。高血糖导致血管损伤的一个重要机制是通过大量的细胞内和细胞外 AGEs(晚期糖基化终产物)的形成。AGEs 是一组异质的蛋白质、脂质和核酸,与还原糖不可逆地交联。AGEs 直接或通过受体介导的机制参与动脉粥样硬化过程,研究最多的受体是 RAGE(AGEs 受体)。AGE-RAGE 相互作用改变细胞信号转导,促进基因表达,并增强促炎分子的释放。它在许多细胞类型中引发氧化应激。在动物研究中充分证明了 AGE-RAGE 相互作用以及导致糖尿病动脉粥样硬化病变发展、进展和不稳定的下游途径在慢性高血糖引起的有害影响中的重要性。此外,在许多人类研究中,AGEs 与糖尿病血管并发症的有害联系已被提出。在本综述中,我们将回顾和批判性评估它们作为糖尿病动脉粥样硬化各个阶段血管损伤的重要介质的作用。

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