The role of TLR4 in the pathogenesis of renal fibrosis and the possible effect of blocking TLR4 signal

我们推测TLR4可能参与了UO诱导的肾损伤的发生，这已被报道在肝纤维化的发病机制中起作用。本研究使用诱导UUO的野生型、缺陷型（TLR4敲除小鼠）和HEJ（TLR4缺陷型）小鼠进行。通过微循环、组织学和分子生物学等指标对各组进行比较，结果提示TLR 4可能与UO所致的早期肾纤维化有关。

We hypothesized that TLR4 might be involved in the development of UO induced renal injury, which has been reported that it plays a role in the pathogenesis of liver fibrosis. The current study was performed using wild type, deficient, (TLR4 knock out mice) and HEJ(TLR4 defective) mice which were inducted UUO. We compared these groups using parameters such as microcirculation, histological and molecular biological methods The results suggested that TLR4 would be related with the early phase of renal fibrosis induced by UO.