Ischemia-reperfusion (I/R) injury is injury caused by a limited blood supply and subsequent blood supply recovery during liver transplantation. Serious ischemia-reperfusion injury is the main cause of transplant failure. Hepatic I/R is characterized by tissue hypoxia due to a limited blood supply and reperfusion inducing oxidative stress and an immune response. Studies have confirmed that Kupffer cells (KCs), resident macrophages in the liver, play a key role in aseptic inflammation induced by I/R. In liver macrophage polarization, M1 macrophages activated by interferon-γ (IFN-γ) and lipopolysaccharide (LPS) exert a pro-inflammatory effect and release a variety of inflammatory cytokines. M2 macrophages activated by IL-4 have an anti-inflammatory response. M1-type KCs are the dominant players in I/R as they secrete various pro-inflammatory cytokines that exacerbate the injury and recruit other types of immune cells via the circulation. In contrast, M2-type KCs can ameliorate I/R through unregulated anti-inflammatory factors. A new notion has been proposed that KC apoptosis may influence I/R in yet another manner as well. Management of KCs is expected to help improve I/R. This review summarizes the effects of hepatic macrophage polarization and apoptosis on liver I/R.

缺血再灌注（I / R）损伤是由于肝移植过程中有限的血液供应和随后的血液供应恢复引起的伤害。严重的缺血再灌注损伤是移植失败的主要原因。肝脏I / R的特征是组织供氧不足，这是由于血液供应有限和再灌注诱导氧化应激和免疫反应所致。研究已经证实，肝脏中的常驻巨噬细胞库普弗细胞（KCs）在由I / R引起的无菌性炎症中起关键作用。在肝巨噬细胞极化中，被干扰素-γ（IFN-γ）和脂多糖（LPS）激活的M1巨噬细胞发挥促炎作用，并释放多种炎性细胞因子。被IL-4激活的M2巨噬细胞具有抗炎反应。M1型KC在I / R中起主要作用，因为它们分泌各种促炎细胞因子，加剧了损伤并通过循环募集了其他类型的免疫细胞。相反，M2型KC可通过不受调节的抗炎因子改善I / R。已经提出了新的观念，即KC凋亡也可以以另一种方式影响I / R。KC的管理有望帮助改善I / R。这篇综述总结了肝巨噬细胞极化和凋亡对肝脏I / R的影响。