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Role of autophagy in megakaryocyte differentiation and platelet formation

机译:自噬在巨核细胞分化和血小板形成中的作用

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Autophagy is a conserved biological process for digestion and recycling of cytoplasmic constituents in eukaryotic cells. Autophagy may trigger cell death or promote cell survival following various forms of stress. The emerging roles of autophagy in megakaryopoiesis, thrombopoiesis, and platelet function have been uncovered using not only in vitro and in vivo genetic models, but also in clinical observations of autophagic structure in patients with thrombocytopenic disorders. Inhibition of autophagy in early stage of megakaryocyte differentiation appears to impede megakaryocyte maturation, reduce platelet formation, and affect platelet function, whereas autophagic deficiency in mature megakaryocytes gives rise to abnormal platelet activation and function without changing platelet size and number. On the other hand, induction of autophagy by rapamycin in megakaryocytes exhibited substantial therapeutic benefits in patients with immune thrombocytopenic purpura (ITP). This mini-review is to highlight recent progresses in understanding the regulation of autophagy in megakaryopoiesis, thrombopoiesis and platelet function to bridge the gap between autophagy and megakaryocyte/platelet pathophysiology.
机译:自噬是一种保守的生物过程,用于消化和再循环真核细胞中的细胞质成分。自噬可能会在各种形式的应激后触发细胞死亡或促进细胞存活。自噬在巨核细胞生成,血小板生成和血小板功能中的新兴作用已不仅在体内和体外遗传模型中发现,而且在血小板减少性疾病患者自噬结构的临床观察中也得到了揭示。抑制巨噬细胞分化早期的自噬似乎会阻碍巨核细胞成熟,减少血小板形成并影响血小板功能,而成熟巨核细胞的自噬缺乏会导致血小板活化和功能异常,而不会改变血小板的大小和数量。另一方面,雷帕霉素在巨核细胞中诱导自噬对免疫性血小板减少性紫癜(ITP)的患者具有实质性的治疗益处。这篇小型综述旨在强调了解巨噬细胞,血小板生成和血小板功能中自噬调节作用的最新进展,以弥合自噬与巨核细胞/血小板病理生理之间的鸿沟。

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