Research progress of iron metabolism and ferroptosis in myeloid neoplasms.
10.3724/zdxbyxb-2024-0211
- Author:
Yudi WANG
1
;
Weiying FENG
2
;
Fudi WANG
3
;
Junxia MIN
4
Author Information
1. Department of Hematology, Shaoxing People's Hospital, Shaoxing 312000, Zhejiang Province, China. 183819142@qq.com.
2. Department of Hematology, Shaoxing People's Hospital, Shaoxing 312000, Zhejiang Province, China.
3. School of Public Health, Zhejiang University School of Medicine, Hangzhou 310058, China.
4. Institute of Translational Medicine, Zhejiang University, Hangzhou 310058, China. junxiamin@zju.edu.cn.
- Publication Type:English Abstract
- Keywords:
Ferroptosis;
Iron metabolism;
Mechanism;
Myeloid neoplasms;
Review
- MeSH:
Ferroptosis;
Humans;
Iron/metabolism*;
Myelodysplastic Syndromes/pathology*;
Reactive Oxygen Species/metabolism*;
Leukemia, Myeloid, Acute/pathology*;
Hepcidins/metabolism*;
Iron Overload/metabolism*;
Myeloproliferative Disorders/metabolism*;
Prognosis
- From:
Journal of Zhejiang University. Medical sciences
2024;53(6):735-746
- CountryChina
- Language:Chinese
-
Abstract:
It is reported that iron metabolism and ferroptosis can influence the occurrence and development of myeloid tumors, which can serve as therapeutic targets. Dysregulation of iron metabolism is present in a variety of myeloid neoplasms. The prognosis of acute myeloid leukemia is related to differential expression of molecules related to iron metabolism. The prognosis of myelodysplastic syndrome patients with iron overload is poor. Myeloproliferative neoplasms are often characterized by the coexistence of iron deficiency and erythrocytosis, which can be treated by targeting hepcidin. Myeloid tumor cells are susceptible to oxidative damage caused by the accumulation of reactive oxygen species and are sensitive to ferroptosis. Ferroptosis has anti-tumor effect in acute myeloid leukemia and myelodysplastic syndrome. Targeting ferroptosis can reverse imatinib resistance in chronic myeloid leukemia. This article reviews the characteristics of iron metabolism in the development and progression of myeloid neoplasms, as well as the mechanism of ferroptosis, to provide a basis for the development of new therapeutic strategies.
