Cellular Signaling Laboratory, Department of Human Anatomical Sciences, University of Bologna, via Irnerio 48, 40126 Bologna, Italy.
J Cell Biochem. 2010 Apr 15;109(6):1065-71. doi: 10.1002/jcb.22483.
Myelodysplastic syndromes (MDS) are defined as clonal hematopoietic stem-cell disorders characterized by ineffective hematopoiesis in one or more of the lineages of the bone marrow. Although distinct morphologic subgroups exist, the natural history of MDS is progression to acute myeloid leukemia (AML). However, the molecular the mechanisms the underlying MDS evolution to AML are not completely understood. Inositides are key cellular second messengers with well-established roles in signal transduction pathways, and nuclear metabolism elicited by phosphoinositide-specific phospholipase C (PI-PLC) beta1 and Akt plays an important role in the control of the balance between cell cycle progression and apoptosis in both normal and pathologic conditions. Recent findings evidenced the role played by nuclear lipid signaling pathways, which could become promising therapeutic targets in MDS. This review will provide a concise and updated revision of the state of art on this topic.
骨髓增生异常综合征（MDS）被定义为造血干细胞克隆性疾病，其特征是骨髓中一个或多个谱系的造血无效。尽管存在明显的形态亚组，但 MDS 的自然病程是进展为急性髓系白血病（AML）。然而，MDS 向 AML 演变的分子机制尚不完全清楚。肌醇是关键的细胞第二信使，在信号转导途径中具有明确的作用，而磷酸肌醇特异性磷脂酶 C（PI-PLC）β1 和 Akt 引发的核代谢在正常和病理条件下控制细胞周期进展和细胞凋亡之间的平衡中起着重要作用。最近的研究结果证实了核脂质信号通路所起的作用，这可能成为 MDS 的有前途的治疗靶点。这篇综述将对这一主题的最新研究进展进行简明扼要的回顾。
