摘要
细胞焦亡(Pyroptosis)是一种新的程序性细胞死亡方式,与骨髓增生异常综合征(MDS)的发生发展密切相关。最新研究表明,S100A9/TLR4,S100A9/CD33及Nox/ROS信号途径能激活氧敏感性NLRP3炎性小体,诱导造血干细胞(HSC)/造血祖细胞(HPC)发生焦亡,导致MDS患者骨髓无效造血。对细胞焦亡在MDS发病过程中的作用及分子机制的深入研究,将为MDS的诊断与治疗提供新的机遇。本文就细胞焦亡在MDS发病过程中作用及分子机制最新研究进展作一综述。
Pyroptosis is a novel type of programmed cell death,which is closely related with the pathogenesis of myelodysplastic syndromes（ MDS）.The recent studies showed that all of S100A9/TLR4,S100A9/CD33 and Nox/ROS signaling pathways can activate oxygen-sensitivity NLRP3 inflammasome and then induce the pyroptosis of hematopoeitic stem cells（ HSC）/hematopeitic pregenitor cells（ HPC）,resulting in ineffective hematopoiesis in patients with MDS.Further studies on the role and molecular mechanism of pyroptosis in the pathogenesis of MDS will provide the potential opportunity for the diagnosis and treatment of MDS.Here,the recent advances in the role and mechnism of pyroptosis in the pathogenesis of MDS are reviewed.
作者
林莹
高清平
叶柏新
LIN Ying;GAO Qing-Ping;YE Bai-Xin(Department of Hematology, People＇s Hospital of Wuhan University, Wahan 430060, Hubei Province, Chin)
出处
《中国实验血液学杂志》
CAS
CSCD
北大核心
2018年第3期937-941,共5页
Journal of Experimental Hematology
基金
国家自然科学基金(81600101)
