Department of Pathology, College of Physicians and Surgeons, Columbia University, New York, NY 10032, USA.
Trends Endocrinol Metab. 2010 Jan;21(1):50-6. doi: 10.1016/j.tem.2009.07.003. Epub 2009 Sep 25.
The multi-ligand Receptor for Advanced Glycation Endproducts (RAGE) is expressed in podocytes and endothelial cells in the human and murine glomerulus. Although present at low levels in homeostasis, RAGE expression is increased during disease. Pharmacological antagonism of RAGE or its genetic deletion imparts marked protection from podocyte effacement, albuminuria and glomerular sclerosis in disease models. In human subjects, associations between specific genetic polymorphisms of RAGE and levels of soluble forms of RAGE are linked to disease states in the kidney. In this review, we summarize the evidence from mouse to man, linking RAGE to the pathogenesis of nephropathy.
多配体受体晚期糖基化终产物 (RAGE) 在人肾小球和鼠肾小球的足细胞和内皮细胞中表达。虽然在稳态下表达水平较低，但在疾病状态下表达增加。RAGE 的药理学拮抗或其基因缺失可显著防止疾病模型中的足细胞消失、白蛋白尿和肾小球硬化。在人类中，RAGE 的特定遗传多态性与可溶性 RAGE 形式的水平之间的关联与肾脏疾病状态有关。在这篇综述中，我们总结了从鼠到人之间的证据，将 RAGE 与肾病的发病机制联系起来。
