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晚期糖基化终产物受体与晚期氧化蛋白产物相互作用诱导足细胞损伤。

Interaction of receptor for advanced glycation end products with advanced oxidation protein products induces podocyte injury.

机构信息

Department of Biochemistry and Molecular Vascular Biology, Kanazawa University Graduate School of Medical Science, Kanazawa, Japan.

出版信息

Kidney Int. 2012 Oct;82(7):733-5. doi: 10.1038/ki.2012.163.

DOI:10.1038/ki.2012.163
PMID:22975994
Abstract

Chronic kidney disease (CKD) is characterized by progressive decline in renal function. Podocyte dropouts contribute to the pathogenesis of diabetic and nondiabetic CKD. Zhou and colleagues demonstrate that the association between advanced oxidation protein products (AOPPs) and receptor for advanced glycation end products (RAGE) elicited podocyte injuries, using cultured podocytes and mice injected with AOPPs. This study suggests that the blockade of RAGE is preventive and therapeutic against podocyte apoptosis caused by oxidative stress-related AOPPs in CKD.

摘要

慢性肾脏病(CKD)的特征是肾功能进行性下降。足细胞丢失导致糖尿病和非糖尿病 CKD 的发病机制。Zhou 及其同事使用培养的足细胞和注射 AOPPs 的小鼠证明,晚期氧化蛋白产物(AOPPs)与晚期糖基化终产物受体(RAGE)之间的关联引起足细胞损伤。这项研究表明,阻断 RAGE 可预防和治疗 CKD 中与氧化应激相关的 AOPPs 引起的足细胞凋亡。

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