期刊文献+

巨核细胞分化与血小板生成机制的研究进展 被引量:5

Recent advances in mechanisms of megakaryopoiesis and platelet formation
原文传递
导出
摘要 血小板为血液循环中发挥止血与血管损伤修复功能的特殊细胞.为机体止血、血栓形成过程中的重要构成因素?其亦涉及机体的炎症反应、固有免疫、血管生成与肿瘤的远处转移等过程。目前已知的血小板生成机制中,骨髓造血干细胞(HSC)与祖细胞经一系列可控的分化、成熟过程生成巨核细胞.而巨核细胞通过生成长分支状的前血小板.延伸穿过骨髓血窦而释放血小板。骨髓腔、细胞外基质及血小板生成素(TPO)等各种细胞因子共同作用.促进冃核细胞分化和血小板生成,为巨核细胞分化的主要调控因素。认识与了解巨核细胞分化、血小板生成的机制.可以为血小板相关疾病的治疗提供坚实的理论基础。笔者拟就目前关于巨核细胞分化及血小板生成机制方面的新研究进展进行综述。 Platelets are specialized cells, which are functioned to prevent bleeding and minimize blood vessel injury, and are also the predominating factor in the processes of hemostasis and thrombosis, while implicate in other processes including inflammation, innate immunity, angiogenesis and tumor metastasis. Among current mechanisms of platelet formation, platelets are produced by megakaryocytes, which are themselves generated by a process of controlled differentiation and maturation of bone marrow hematopoietic stem cells (HSC) and progenitor cells. Megakaryocytes release platelets by extending long, branching proplatelets, into sinusoidal blood vessels. Bone marrow cavity and extracellular matrix composition together with cytokines as thrombopoietin (TPO) are key regulators of megakaryopoiesis by supporting cell differentiation and platelet formation. Understanding the mechanisms of megakaryocyte differentiation and platelet formation can provide a solid theoretical basis for the treatment of platelet-related diseases. This review summarizes the current scientific research progress in the mechanisms of megakaryopoiesis and thrombopoiesis.
作者 李蓉蔚 杨仁池 Li Rongwei;Yang Renchi(Thrombosis and Hemostasis Centre,Institute of Hematology and Blood Diseases Hospital * Chinese Academy of Medical Sciences & Peking Union Medical College,Tianjin 300020 ,China)
出处 《国际输血及血液学杂志》 CAS 2019年第1期30-35,共6页 International Journal of Blood Transfusion and Hematology
基金 国家自然科学基金项目(81670118).
关键词 巨核细胞 细胞分化 血小板生成 转录因子 细胞凋亡 巨核细胞分化 Megakaryocytes Cell differentiation Thrombopoiesis Transcription factors Apoptosis Megakaryopoiesis
  • 相关文献

同被引文献55

引证文献5

二级引证文献4

相关作者

内容加载中请稍等...

相关机构

内容加载中请稍等...

相关主题

内容加载中请稍等...

浏览历史

内容加载中请稍等...
;
使用帮助 返回顶部