Targetting ferroptosis for blood cell-related diseases

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.

Keywords:

• Ferroptosis
• anaemia
• leukaemia
• thromboembolism
• infectious diseases

Acknowledgements

Authors are very grateful to Professor Linxi Chen and Professor Nian Fu for helping to formulate the theme and framework for this review.

Authors contributions

Zhe Chen wrote the manuscript. Jinyong Jiang was responsible for language modification and correction. Professor Linxi Chen and Professor Nian Fu illuminated instruction and expert advice for this paper.

Disclosure statement

The authors declare that they have no conflicts of interest.

Additional information

Funding

This study was supported by the National Natural Science Foundation of China (81973326) and the Natural Science Foundation of Hunan Province (2019JJ50523).