摘要
病理性骨丢失疾病(骨溶解、佩吉特病)通常是由破骨细胞过度分化和活性引起的。据报道,Rho GTPases家族成员Rac1/2 (Rac1和Rac2)在破骨细胞分化过程中发挥多种细胞功能方面具有特殊作用,包括对动态肌动蛋白细胞骨架重排的最显著作用。此外,越来越多的研究表明Rac1/2对破骨细胞骨架组织的调节作用是通过GEFs成员Dock5实现的。尽管关于这一主题的相关研究的数量仍然有限,但是已经报道了几个优秀的研究,这些研究广泛地探索了在破骨细胞生成调节过程中涉及Rac1/2和Dock5的分子机制,以及它们作为骨丢失疾病的治疗靶点的作用。在这篇综述中,我们旨在关注最近的研究进展,以广泛了解Rho GTPases Rac1/2和Dock5在破骨细胞生成中的作用,以及它们作为调节破骨细胞生成的潜在治疗靶点的作用。
关键词: Rac1,Rac2,Dock5,破骨细胞生成,骨稳态,分子。
图形摘要
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