Gu Lijuan, Tao Yu, Chen Cheng, Ye Yingze, Xiong Xiaoxing, Sun Yao
Central Laboratory, Renmin Hospital of Wuhan University, Wuhan, 430060, China.
Department of Nephrology, Renmin Hospital of Wuhan University, Wuhan, 430060, China.
Int Urol Nephrol. 2018 Nov;50(11):2027-2035. doi: 10.1007/s11255-018-1918-6. Epub 2018 Jul 4.
Ischemia/reperfusion injury (IRI) occurs commonly during renal transplantation. It has been well demonstrated that the inflammatory response has an important role in the pathogenesis and pathological processes of IRI. However, the signaling events that trigger the activation of the inflammatory response are less clear. Accumulated evidence has identified the role of various injury factors released from or exposed in ischemic, damaged, or dying cells, which serve as initiators of the inflammatory response and exacerbate kidney injury after renal IRI. Signaling pathways triggered by these endogenous molecules that activate different pathogen recognition receptors have also been widely investigated. Here, we review the molecular signaling molecules that initiate the inflammatory response during renal IRI and that provide potential therapeutic options for the disease.
缺血/再灌注损伤（IRI）在肾移植过程中很常见。已有充分证据表明，炎症反应在IRI的发病机制和病理过程中起重要作用。然而，触发炎症反应激活的信号事件尚不清楚。越来越多的证据表明，缺血、受损或濒死细胞释放或暴露的各种损伤因子起了作用，这些因子作为炎症反应的启动因子，会加重肾IRI后的肾损伤。由这些内源性分子触发的激活不同病原体识别受体的信号通路也得到了广泛研究。在此，我们综述了在肾IRI期间引发炎症反应并为该疾病提供潜在治疗选择的分子信号分子。
