A breakthrough in diabetic nephropathy: the role of endothelial dysfunction.
A breakthrough in diabetic nephropathy: the role of endothelial dysfunction.
复制标题
糖尿病肾病的突破：内皮功能障碍的作用。
DOI：
10.1093/ndt/gfm380
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发表时间：
2007
期刊：
影响因子：
--
通讯作者：
Johnson,RichardJ
中科院分区：
文献类型：
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作者：
Nakagawa,Takahiko;Segal,Mark;Croker,Byron;Johnson,RichardJ
Kanetsuna等人[1]已经在美国病理学杂志上发表了一篇重要论文，报道了在遗传上缺乏内皮型一氧化氮合酶（eNOS）的糖尿病小鼠（用链脲佐菌素）中可以诱导类似于人类糖尿病肾病的肾脏病变。eNOS是内皮细胞中产生一氧化氮（NO）的关键酶。反过来，NO在脉管系统中具有多种功能，包括充当血管扩张剂、抗炎、抗血栓形成和抗增殖活性。在这项研究中，糖尿病eNOS敲除小鼠出现了与人类糖尿病肾病一致的肾功能（蛋白尿，肾小球滤过率降低）和结构变化。迄今为止，在小鼠中难以建立类似于人类疾病的糖尿病肾病模型，因此本文代表了对糖尿病肾病发病机制的突破。
Kanetsuna et al.[1] have published an important paper in the American Journal of Pathology, reporting that renal lesions resembling human diabetic nephropathy can be induced in mice made diabetic (with streptozotocin) which genetically lack endothelial nitric oxide synthase (eNOS). eNOS is a key enzyme in endothelial cells that produces nitric oxide (NO). In turn, NO has multiple functions in the vasculature, including acting as a vasodilator, anti-inflammatory, anti-thrombotic and anti-proliferative activities. In this study, diabetic eNOS knockout mice developed both renal functional (proteinuria, reduced glomerular filtration rate) and structural changes consistent with human diabetic nephropathy. Up to now, it has been difficult to develop in mice models of diabetic nephropathy that resemble human disease, so this article represents a breakthrough in the pathogenesis of diabetic nephropathy.