The role of Janus tyrosine kinase(JAK) signal transducer and activator of transcription(STAT) and suppressor of cytokine signaling (SOCS) pathway in the renal interstitial fibrosis after unilateral ureteral obstruction

JAK/STAT信号通路对单侧输尿管梗阻小鼠肾纤维化的保护作用JAK/STAT系统是一条重要的细胞内信号通路，参与多种细胞因子和刺激物的调节，参与多种炎症反应、增殖和分化。SOCS作为该系统的负反馈通路发挥作用。JAK/STAT/SOCS系统可能在肾脏反应中起重要作用。为了阐明JAK/STAT/SOCS系统如何参与肾纤维化，在存在或不存在JAK标记物掺入的纳米颗粒（吡啶6-PGLA）的情况下，在BALB/c或SOCS 3杂合敲除（SOCS 3 +/-）小鼠中诱导单侧输尿管梗阻（UUO）。本研究提示JAK/STAT 3信号通路可能通过激活MMP-2在UUO肾纤维化修复过程中发挥重要作用。

Protective role of JAK/STAT signaling against renal fibrosis in mice with unilateral ureteral obstructionJAK/STAT system is an essential intracellular signaling pathway of various cytokines and stimuli that could regulate a variety of inflammatory reactions, proliferation, and differentiation. SOCS work as a negative feedback pathway of this system. JAK/STAT/SOCS system may play an important role in renal responses. To clarify how JAK/STAT/SOCS system was involved in renal fibrosis, unilateral ureteral obstruction (UUO) was induced in BALB/c or SOCS3 heterozygous knockout (SOCS3+/-) mice in the presence or absence of JAK inhibitor-incorporated nanoparticle (pyridine6-PGLA). Our present study suggests that JAK/STAT3 signaling may play an important role in repair process of renal fibrosis in UUO partly via activation of MMP-2.