Hou Jincheng, Li Chenghao, Li Geng, Yim Wai Yen, Geng Bingchuan, Cheng Yuqi, Wang Zihao, Fan Zhengfeng, Tong Fuqiang, Shi Jiawei, Wang Yixuan, Dong Nianguo
Department of Cardiovascular Surgery, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
Key Laboratory of Organ Transplantation, Ministry of Education, National Health Commission (NHC) Key Laboratory of Organ Transplantation, Key Laboratory of Organ Transplantation, Chinese Academy of Medical Sciences, Wuhan, China.
Front Immunol. 2025 May 23;16:1604429. doi: 10.3389/fimmu.2025.1604429. eCollection 2025.
Organ transplantation is a critical treatment for end-stage organ failure, but long-term graft survival remains suboptimal due to ischemia-reperfusion injury (IRI) and transplant rejection. The immune microenvironment, especially macrophages, plays a key role in these processes. Various forms of regulated cell death (apoptosis, autophagy, pyroptosis, ferroptosis, necroptosis) in macrophages significantly influence transplant rejection by mediating cellular communication and shaping the immune microenvironment. Apoptosis, pyroptosis, ferroptosis and necroptosis in macrophages exacerbate graft rejection while autophagy in macrophages protects against transplant rejection by reducing inflammation.This paper reviews the specific molecular mechanisms of macrophage regulated cell death, their impact on the IRI and transplant rejection, thus further provide potential therapeutic target for improving transplant outcomes.
器官移植是终末期器官衰竭的关键治疗方法，但由于缺血再灌注损伤（IRI）和移植排斥反应，长期移植物存活仍不尽人意。免疫微环境，尤其是巨噬细胞，在这些过程中起着关键作用。巨噬细胞中各种形式的程序性细胞死亡（凋亡、自噬、焦亡、铁死亡、坏死性凋亡）通过介导细胞间通讯和塑造免疫微环境，显著影响移植排斥反应。巨噬细胞中的凋亡、焦亡、铁死亡和坏死性凋亡会加剧移植物排斥反应，而巨噬细胞中的自噬则通过减轻炎症来预防移植排斥反应。本文综述了巨噬细胞程序性细胞死亡的具体分子机制、它们对IRI和移植排斥反应的影响，从而进一步为改善移植结局提供潜在的治疗靶点。
