国际肿瘤学杂志 ›› 2026, Vol. 53 ›› Issue (9): 566-571.doi: 10.3760/cma.j.cn371439-20251106-00090

• 综述 • 上一篇    下一篇

铁代谢调控骨髓增生异常疾病的研究进展

江金霞, 张学忠(), 杨斐斐()   

  1. 南京医科大学附属南京医院 南京市第一医院血液科, 南京 210001
  • 收稿日期:2025-11-06 出版日期:2026-09-08 发布日期:2026-08-25
  • 通讯作者: 杨斐斐,Email:lydia9017@sina.com;
    张学忠,Email:zxuezhong1968@sina.com
  • 基金资助:
    国家自然科学基金(82000160);南京市卫生科技发展项目(YKK21138)

Research progress on the regulation of iron metabolism in myelodysplastic diseases

Jiang Jinxia, Zhang Xuezhong(), Yang Feifei()   

  1. Department of Hematology, Nanjing First Hospital,Affiliated Nanjing Hospital of Nanjing Medical University, Nanjing 210001, China
  • Received:2025-11-06 Online:2026-09-08 Published:2026-08-25
  • Contact: Yang Feifei,Email:lydia9017@sina.com;
    Zhang Xuezhong,Email:zxuezhong1968@sina.com
  • Supported by:
    National Natural Science Foundation of China(82000160);Health Technology Development Project of Nanjing of China(YKK21138)

摘要:

骨髓增生异常综合征和费城染色体阴性骨髓增殖性肿瘤同属骨髓增生异常疾病,均为起源于造血干细胞的克隆性髓系细胞疾病,呈显著异质性,以无效造血、白血病转化风险增高为主要特征。铁代谢紊乱可通过多种机制驱动疾病进展。在骨髓增生异常综合征中,铁过载可导致活性氧增多、凋亡蛋白酶激活因子-1上调和生长分化因子11水平升高,从而抑制骨髓造血干/祖细胞增殖,增加白血病转化风险。铁代谢紊乱还可通过异常激活红细胞生成过程中的STAT5信号转导加重真性红细胞增多症患者疾病恶化,影响原发性血小板增多症及骨髓纤维化患者预后。深入分析铁稳态失衡在骨髓增生异常疾病中的作用机制,可为后续开发靶向铁代谢精准治疗策略提供重要依据。

关键词: 骨髓增生异常综合征, 骨髓增生异常-骨髓增殖性疾病, 铁代谢障碍, 治疗

Abstract:

Both myelodysplastic syndromes and Philadelphia chromosome-negative myeloproliferative neoplasms are clonal myeloid disorders originating from hematopoietic stem cells,classified under myelo-proliferative and myelodysplastic diseases. They exhibit considerable heterogeneity and are primarily characterized by ineffective hematopoiesis and an elevated risk of leukemic transformation. Dysregulated iron metabolism contributes to disease progression through multiple mechanisms. In myelodysplastic syndromes,iron overload leads to increased reactive oxygen species,elevation of apoptotic protease-activating factor 1,and elevated growth differentiation factor 11 levels,thereby suppressing the proliferation of hematopoietic stem/progenitor cells and augmenting the risk of leukemic transformation. Furthermore,iron metabolism dysregulation exacerbates disease progression in polycythemia vera patients by aberrantly activating STAT5 signaling during erythropoiesis,and adversely affects the prognosis of those with essential thrombocythemia and myelofibrosis. A thorough investigation into the mechanisms of iron homeostasis imbalance in myelodysplastic/myeloproliferative diseases provides a critical foundation for the subsequent development of targeted and precise therapeutic strategies for iron metabolism.

Key words: Myelodysplastic syndromes, Myelodysplastic-myeloproliferative diseases, Iron metabolism disorders, Therapy