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肝缺血再灌注损伤(HIRI)作为肝移植术等肝脏外科手术后不可避免的并发症，会导致术后肝功能损伤甚至肝衰竭，威胁患者生命。巨噬细胞作为免疫细胞中的重要组成成分，在HIRI过程中具有关键作用。肝驻留巨噬细胞(KCs)发生极化后，其在HIRI过程中起着完全相反的作用。KCs向M2型细胞极化拮抗了M1型极化所导致的促炎反应，从而保护肝损伤。KCs向M1或M2极化的信号通路至今尚未完全清楚。M2型极化作用的深入阐明可进一步指导后续靶向药物的研发，对缓解或治愈HIRI有着重要作用。笔者对HIRI中与KCs的M2型极化作用相关的应用以及可能参与的信号通路进行归纳总结，为今后临床靶向药物的研发提供参考。

Hepatic ischemia-reperfusion injury (HIRI), as an unavoidable complication after liver surgery such as liver transplantation, can lead to postoperative hepatic impairment or even hepatic failure, which threatens patients' lives. As an important component of immune cells, macrophages have a key role in the process of HIRI. The polarization of liver resident Kupffer cells (KCs) plays a completely opposite role in HIRI. The polarization of KCs toward M2 cells antagonizes the pro-inflammatory response caused by M1 polarization and thus protects against liver injury. However, the signaling pathways of KCs polarized toward M1 or M2 are not yet fully understood. The in-depth elucidation of the role of M2 type polarization can further guide the development of subsequent targeted drugs, which will play an important role in alleviating or curing HIRI. The authors summarize the relevant applications and possible signaling pathways involved in the role of M2-type polarization of hepatic macrophages in HIRI, which will provide references for the development of clinically targeted drugs in the future.