Elucidation of the mechanisms underlying podocyte injury through endoplasmic reticulum stress and Development of novel therapeutic strategies for glomerular diseases

探讨内质网应激在足细胞损伤过程中的意义。培养的生长受限足细胞在低氧条件下表现出增强的未折叠蛋白反应，这是我们测试的代谢压力之一。CHOP是内质网应激相关分子之一，其相关的细胞凋亡途径与Bcl2相关蛋白组成了一个复杂的网络。此外，我们发现甲基乙二醛，一种羰基化合物，直接损伤足细胞。这些结果提示，缺氧、内质网应激和羰基应激可能相互串扰，促进足细胞损伤。

We investigated the implication of endoplasmic reticulum(ER) stress in the process of podocyte injury. Cultured growth-restrictive podocytes showed enhanced unfolded protein response under hypoxia, one of the metabolic stresses we tested. The apoptosis pathway associated with CHOP, which is one of the ER stress-related molecules, included a complicated network with Bcl-2-related proteins. Furthermore, we found that methylglyoxal, a carbonyl compound, directly damaged podocytes. Those results suggest that hypoxia, ER stress and carbonyl stress may have a crosstalk with each other and promote podocyte injury.