论文摘要
骨髓纤维化伴髓样化生（myelofibrosis with myeloid metaplasia）是一种病因不明,进行性结缔组织取代正常骨髓造血组织,伴骨髓外化生的骨髓增殖性疾病。目前其发病机理尚未明确,但多数学者认为MMM是一种造血干细胞克隆性疾病,而骨髓纤维化、新生血管形成、骨硬化等骨髓微环境改变则是属于继发反应。患者的直接致死亡原因常为骨髓纤维化导致的骨髓功能衰竭而不是原发的造血干细胞的异常。目前的药物治疗主要是对症性的,尚难明显改变患者骨髓纤维化的进程。因此以阻断MMM患者骨髓纤维化的进程为目标的治疗方法正日益受到大家的关注。 病理组织学显示骨髓纤维化患者骨髓组织中充满大量成纤维细胞并伴有胶原蛋白的沉积,进一步的研究表明这些骨髓成纤维细胞的大量增殖是受异常增殖分化的巨核细胞、单核细胞及其分泌的细胞因子如PDGF、bFGF、EGF和转化生长因子-β（TGF-β 1）等调控。其中TGF-β很早就被认为在多种组织脏器的纤维化中具有重要作用。在骨髓纤维化的研究中,也有学者将携带促血小板生成素（Thrombopoietin,TPO）编码的腺病毒导入两种来源的鼠造血干细胞（不表达TGF-β 1的纯合子干细胞和表达TGF-β 1的野生型干细胞）,当给试验鼠植入不表达TGF-β 1的纯合子干细胞后,骨髓组织内未见到任何网状纤维沉积;
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