Brosius Frank C, Khoury Charbel C, Buller Carolyn L, Chen Sheldon
Departments of Internal Medicine and Molecular and Integrative Physiology, University of Michigan Medical School, 5520 MSRB1, 1150 W. Medical Center Drive, Ann Arbor, MI 48109-0680, USA, Tel.: +1 734 764 3157, ,
Expert Rev Endocrinol Metab. 2010;5(1):51-64. doi: 10.1586/eem.09.70.
Diabetic nephropathy (DN) is characterized by a plethora of signaling abnormalities that together ultimately result in the clinical and pathologic hallmarks of DN, namely progressive albuminuria followed by a gradual decline in glomerular filtration rate leading to kidney failure, and accompanied by podocyte loss, progressive glomerular sclerosis and, ultimately, progressive tubulointerstitial fibrosis. Over the past few years, the general understanding of the abnormalities in signaling pathways that lead to DN has expanded considerably. In this review, some of the important pathways that appear to be involved in driving this process are discussed, with special emphasis on newer findings and insights. Newer concepts regarding signaling changes in bradykinin, mTOR, JAK/STAT, MCP-1, VEGF, endothelial nitric oxide synthase, activated protein C and other pathways are discussed.
糖尿病肾病（DN）的特征是存在大量信号异常，这些异常最终共同导致DN的临床和病理特征，即进行性蛋白尿，随后肾小球滤过率逐渐下降，导致肾衰竭，并伴有足细胞丢失、进行性肾小球硬化，最终出现进行性肾小管间质纤维化。在过去几年中，对导致DN的信号通路异常的总体认识有了很大扩展。在本综述中，将讨论一些似乎参与驱动这一过程的重要通路，特别强调新的发现和见解。还将讨论关于缓激肽、mTOR、JAK/STAT、MCP-1、VEGF、内皮型一氧化氮合酶、活化蛋白C和其他通路信号变化的新概念。
