与颅缝病理生理学相关的信号机制:颅缝闭合

Maria A. Katsianou , Christos Adamopoulos , Heleni Vastardis , Efthimia K. Basdra
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引用次数: 53

摘要

正常的延伸和颅骨扩张是一个同步的过程,普遍沿着颅骨缝合线的成骨交叉点。颅骨缝合线作为骨生长部位,允许在骨前缘边缘快速生成骨,同时保持专利。一个或多个颅骨缝合线的过早融合可引发颅缝闭闭,这是一种以外观和功能障碍的戏剧性表现为特征的出生缺陷。直到今天,手术矫正是唯一的修复措施颅缝闭锁相关的相当高的死亡率。临床研究已经确定了几个与颅缝愈合综合征发病机制有关的基因,对决定缝合命运的潜在分子信号事件有了有用的见解。在这篇综述中,我们利用与缝合病理生物学有关的细胞内信号转导途径,试图确定治疗靶向的关键信号分子。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Signaling mechanisms implicated in cranial sutures pathophysiology: Craniosynostosis

Normal extension and skull expansion is a synchronized process that prevails along the osteogenic intersections of the cranial sutures. Cranial sutures operate as bone growth sites allowing swift bone generation at the edges of the bone fronts while they remain patent. Premature fusion of one or more cranial sutures can trigger craniosynostosis, a birth defect characterized by dramatic manifestations in appearance and functional impairment. Up until today, surgical correction is the only restorative measure for craniosynostosis associated with considerable mortality. Clinical studies have identified several genes implicated in the pathogenesis of craniosynostosis syndromes with useful insights into the underlying molecular signaling events that determine suture fate. In this review, we exploit the intracellular signal transduction pathways implicated in suture pathobiology, in an attempt to identify key signaling molecules for therapeutic targeting.

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