Chang Wilson J, Toledo-Pereyra Luis H
Department of Research and Surgery, Kalamazoo Center for Medical Studies, Michigan State University, Kalamazoo, Michigan, USA.
J Invest Surg. 2012 Aug;25(4):271-7. doi: 10.3109/08941939.2012.687802.
Liver ischemia-reperfusion (I/R) injuries are significant clinical challenges implicated in various hepatic surgical procedures and transplantations. Associated with varying degrees of insult, the hallmark of I/R is the excessive inflammatory response potentiated by the host immune system. Toll-like receptors (TLRs), known to play an important role in pathogen-derived inflammation, are now thought to participate in I/R injury-derived inflammation signaling pathways. Endogenous particles (proteins, cytokines, nucleic acids) that are released from damaged host cells bind to TLR2, TLR4, and TLR9, resulting in even further injury by subsequent inflammatory reactions and activation of the innate immune system. This review aims to systematically examine the current literature about TLR signaling mechanisms, allowing for a greater understanding of the precise role of TLRs in hepatic I/R injuries.
肝脏缺血再灌注(I/R)损伤是各类肝脏外科手术和移植中面临的重大临床挑战。I/R与不同程度的损伤相关,其标志是宿主免疫系统增强的过度炎症反应。Toll样受体(TLR)在病原体引发的炎症中发挥重要作用,现在认为其参与I/R损伤引发的炎症信号通路。受损宿主细胞释放的内源性颗粒(蛋白质、细胞因子、核酸)与TLR2、TLR4和TLR9结合,通过后续炎症反应和先天免疫系统的激活导致更严重的损伤。本综述旨在系统研究关于TLR信号机制的现有文献,以便更深入了解TLR在肝脏I/R损伤中的精确作用。