IL6／STAT3信号通路在肝脏缺血再灌注损伤中的作用研究进展

Research advances in the role of IL-6/STAT3 signaling pathway in hepatic ischemia-reperfusion injury

肝脏缺血再灌注损伤（HIR）的发生发展具有重要临床意义。IL-6与HIR密切相关，对下游信号传导转录和激活因子3（STAT3）间的信号通路也具有重要作用。IL-6一直被认为是一个典型的促炎性细胞因子，它通过gp130的同源二聚体化激活Janus激酶（JAK）／STAT信号转导通路参与炎症疾病的发生发展。然而，近十年的研究表明IL-6不仅可与其可溶性受体结合（反式信号通路）并介导HIR，并且还可与其膜结合受体结合（经典信号通路）介导再生与抗炎等保护性作用。本文对IL-6／STAT3信号通路在肝脏缺血再灌注损伤研究领域的最新进展进行综述。

The occurrence and development of hepatic isehemia-reperfusion injury （HIR） has important clinical signifi- cance, while interleukin-6 （IL-6） is closely related to HIR and it plays an important role in the signaling pathway between down- stream signal transducer and activator of transcription 3 （STAT3）. IL-6 has been considered to be a typical proinflam- matory eytokine. Activation of the gpl30 homodimer by IL-6 leads to the initiation of Janus kinase （JAK）-STAT path-way that is often constitutively switched on in inflammatory diseases. However, a plethora of studies in the last decade showed that only signaling via the soluble IL-6R （trans-signaling） accounts for the deleterious effects of IL-6, whereas the signaling via the membrane-bound receptor （classic signaling） is essential for the regenerative and anti-inflammatory effects of IL-6. In this paper,the latest progresses in the research field of the IL-6/STA33 sig- naling pathway in HIR is discussed.