细胞焦亡在骨髓增生异常综合征发生中作用机制的研究进展  

Research progress on role of pyroptosis in pathogenesis of myelodyplastic syndrome

作　　者：凌春 金其川[1] 宫文玉 张启国[2] Ling Chun;Jin Qichuan;Gong Wenyu;Zhang Qiguo(Department of Hematology,the First People's Hospital of Chuzhou ,Chuzhou 239100,Anhui Province, China;Drum Tower Hospital,Medical School of Nanjing University, Nanjing 210008,Jiangsu Province,China)

机构地区：[1]安徽省滁州市第一人民医院,239100 [2]南京大学医学院附属鼓楼医院,210008

出　　处：《国际输血及血液学杂志》2018年第6期535-538,共4页International Journal of Blood Transfusion and Hematology

摘　　要：细胞焦亡是一种依赖于半胱氨酸天冬氨酸蛋白酶(Caspase)的细胞程序性死亡方式。多种细胞内、外病原体通过活化Caspase-1和Caspase-4/5/11,以及激活白细胞介素(IL)-1β和IL -18的前体,促进机体炎性小体形成,引起细胞裂解及更多炎症因子的释放,最终导致细胞炎症性死亡。细胞焦亡过程中炎性小体的产生,Toll样受体(Toll like receptor ,TLR)信号通路及骨髓微环境的改变,形成炎症环境,从而诱发骨髓增生异常综合征(MDS)。笔者拟就细胞焦亡的相关机制及其在MDS发生中的作用进行综述。Pyroptosis is the programmed cell death mediated by inflammatory cysteine-aspartic protease (Caspase). Intercallular or extracellular pathogens can promote the formation of inflammatory by activating Caspase-1, Caspase-4/5/11, pro-interleukin (IL)-1β and pro-IL-18. The activated inflammatory cytokines lead to cell lysis and inflammatory factors release, and finally induced cell death.The alterations of Toll like receptor(TLR) signaling pathway and bone microenvironment, and presence of inflammasome could cause the formation of an inflammatory environment, leading to myelodyplastic syndrome (MDS). The article reviews the mechanism of pyroptosis and the relationship between pyroptosis and MDS.

关 键 词：细胞焦亡 骨髓增生异常综合征 半胱氨酸天冬氨酸蛋白酶 白细胞介素1Β 白细胞介素18 

分 类 号：R551.3[医药卫生—血液循环系统疾病]