Abstract

Ferroptosis is an iron-dependent cell death pathway and participates in various diseases. Current evidence suggests that ferroptosis can obviously affect the function of blood cells. This paper aims to elaborate the role of ferroptosis in blood cells and related diseases. First, abnormal ferroptosis damages the developing red blood cells by breaking systemic iron homeostasis, leading to erythropoiesis suppression and anaemia. Ferroptosis mediates neutrophils recruitment and neutrophil extracellular trap formation (NETosis). In T-cells, ferroptosis induces a novel point of synergy between immunotherapy and radiotherapy. Additionally, ferroptosis may mediate B cells differentiation, antibody responses and lymphoma. Nevertheless, increased ferroptosis can ameliorate acute myeloid leukaemia and T-cell leukaemia/lymphoma by inducing iron-dependent cancer cells death. Besides, ferroptosis activates platelets by increasing P-selectin, thus causing thromboembolism. Ferroptosis mediates virus infection and parasite infection by driving T-cell death and preventing T-cell immunity. Interestingly, ferroptosis is also considered as a critical player in COVID-19 infections, while targetting ferroptosis may also improve thromboembolism and prognosis in patients with COVID-19 infection. Overall, the crucial role of ferroptosis in blood cells will show a new therapeutic potential in blood cell-related diseases.

• Highlights

• Ferroptosis shows a new therapeutic potential for blood cell-related diseases.

• Ferroptosis damages erythropoiesis and thus induces anaemia.

• Ferroptosis induces platelet activation and leads to thromboembolism.

• Ferroptosis regulates T-cell and B-cell immunity, which participant in infectious diseases.

• Inversely, ferroptosis ameliorates acute myeloid leukaemia and T-cell leukaemia.

摘要

铁死亡是一种铁依赖性细胞死亡途径，参与多种疾病。目前的证据表明，铁死亡可以明显影响血细胞的功能。本文旨在阐述铁死亡在血细胞及相关疾病中的作用。首先，异常的铁死亡通过破坏全身铁稳态来破坏发育中的红细胞，导致红细胞生成抑制和贫血。铁死亡介导中性粒细胞募集和中性粒细胞胞外陷阱形成（NETosis）。在 T 细胞中，铁死亡诱导了免疫疗法和放射疗法之间的新协同作用点。此外，铁死亡可能介导 B 细胞分化、抗体反应和淋巴瘤。尽管如此，增加的铁死亡可以通过诱导铁依赖性癌细胞死亡来改善急性髓性白血病和 T 细胞白血病/淋巴瘤。此外，铁死亡通过增加P-选择素激活血小板，从而引起血栓栓塞。铁死亡通过驱动 T 细胞死亡和阻止 T 细胞免疫来介导病毒感染和寄生虫感染。有趣的是，铁死亡也被认为是 COVID-19 感染的关键因素，而针对铁死亡也可能改善 COVID-19 感染患者的血栓栓塞和预后。总体而言，铁死亡在血细胞中的关键作用将在血细胞相关疾病中显示出新的治疗潜力。铁死亡通过驱动 T 细胞死亡和阻止 T 细胞免疫来介导病毒感染和寄生虫感染。有趣的是，铁死亡也被认为是 COVID-19 感染的关键因素，而针对铁死亡也可能改善 COVID-19 感染患者的血栓栓塞和预后。总体而言，铁死亡在血细胞中的关键作用将在血细胞相关疾病中显示出新的治疗潜力。铁死亡通过驱动 T 细胞死亡和阻止 T 细胞免疫来介导病毒感染和寄生虫感染。有趣的是，铁死亡也被认为是 COVID-19 感染的关键因素，而针对铁死亡也可能改善 COVID-19 感染患者的血栓栓塞和预后。总体而言，铁死亡在血细胞中的关键作用将在血细胞相关疾病中显示出新的治疗潜力。

• 强调

• 铁死亡显示了血细胞相关疾病的新治疗潜力。

• 铁死亡会损害红细胞生成，从而导致贫血。

• 铁死亡诱导血小板活化并导致血栓栓塞。

• 铁死亡调节参与传染病的 T 细胞和 B 细胞免疫。

• 相反，铁死亡可改善急性髓性白血病和 T 细胞白血病。