Molecular analysis of the pathophysiology basis of nephrotic syndrome

为了阐明肾病综合征尤其是FSGS的病理生理机制，我们研究了肌球蛋白IIA。首先，我们确定了肌球蛋白IIA的精确定位；肌球蛋白IIA位于足部原突和细胞体中。在表现为重度蛋白尿的人类肾脏疾病中，只有FSGS患者的肾脏标本中myosin IIA的表达水平下降，而其他肾脏疾病患者的肾脏标本中myosin IIA的表达水平没有变化。在大鼠PAN肾病模型中，肌球蛋白IIA在第11天重度蛋白尿时表达水平下降。综上所述，肌球蛋白IIA在人类特发性肾病综合征，特别是FSGS的发展中起着非常重要的作用。

To lucidate the pathophysiology of nephrotic syndrome, especially FSGS, we investigated myosin IIA. First, We determined the precise localization of myosin IIA; myosin IIA is located at the primary process and cell body of podocye. In human kidney diseases manifesting heavy proteinuria, only in the kidney specimen from the patients with FSGS, the level of expression o myosin IIA was decreased, while in those from other kidney disease patients were not changed. In rat PAN nephrosis model, the expression level of myosin IIA was decreased at day 11 when heavy proteinuria was observed. Taken together, myosin IIA play the very important role in the development of human idiopathic nephrotic syndrome, especially FSGS.