Transplantation is a life-saving therapy for patients with end-stage organ disease. Successful outcomes after transplantation require mitigation of the post-transplant inflammatory response, limiting alloreactivity, and prevention of organ rejection. Traditional immunosuppressive regimens aim to dampen the adaptive immune response; however, recent studies have shown the feasibility and efficacy of targeting the innate immune response. Necroinflammation initiated by donor organ cell death is implicated as a critical mediator of primary graft dysfunction, acute rejection, and chronic rejection. Ferroptosis is a form of regulated cell death that triggers post-transplantation inflammation and drives the activation of both innate and adaptive immune cells. There is a growing acceptance of the clinical relevance of ferroptosis to solid organ transplantation. Modulating ferroptosis may be a potentially promising strategy to reduce complications after organ transplantation.

移植是终末期器官疾病患者的一种挽救生命的疗法。移植后的成功结果需要减轻移植后炎症反应、限制同种异体反应性并预防器官排斥。传统的免疫抑制疗法旨在抑制适应性免疫反应；然而，最近的研究表明针对先天免疫反应的可行性和有效性。由供体器官细胞死亡引发的坏死性炎症被认为是原发性移植物功能障碍、急性排斥和慢性排斥的关键介质。铁死亡是一种受调节的细胞死亡形式，可引发移植后炎症并驱动先天性和适应性免疫细胞的激活。人们越来越多地接受铁死亡与实体器官移植的临床相关性。调节铁死亡可能是减少器官移植后并发症的一种潜在有前途的策略。