The vascular network is established and maintained through the processes of vasculogenesis and angiogenesis, which are tightly regulated during embryonic and postnatal life. The formation of a functional vasculature requires critical cellular mechanisms, such as cell migration, proliferation and adhesion, which are dependent on the activity of small Rho GTPases, controlled in part by the dedicator of cytokinesis (DOCK) protein family. Whilst the majority of DOCK proteins are associated with neuronal development, a growing body of evidence has indicated that members of the DOCK family may have key functions in the control of vasculogenic and angiogenic processes. This is supported by the involvement of several angiogenic signalling pathways, including chemokine receptor type 4 (CXCR4), vascular endothelial growth factor (VEGF) and phosphatidylinositol 3-kinase (PI3K), in the regulation of specific DOCK proteins. This review summarises recent progress in understanding the respective roles of DOCK family proteins during vascular development. We focus on existing in vivo and in vitro models and known human disease phenotypes and highlight potential mechanisms of DOCK protein dysfunction in the pathogenesis of vascular disease.

血管网络是通过血管生成和血管生成过程建立和维持的，这些过程在胚胎和出生后受到严格调节。功能性脉管系统的形成需要关键的细胞机制，例如细胞迁移、增殖和粘附，这些机制依赖于小 Rho GTPases 的活性，部分由胞质分裂专用因子 (DOCK) 蛋白家族控制。虽然大多数 DOCK 蛋白与神经元发育有关，但越来越多的证据表明 DOCK 家族的成员可能在控制血管生成和血管生成过程中具有关键功能。这得到了几种血管生成信号通路的支持，包括趋化因子受体 4 型 (CXCR4)，血管内皮生长因子 (VEGF) 和磷脂酰肌醇 3-激酶 (PI3K) 在特定 DOCK 蛋白的调节中。本综述总结了了解 DOCK 家族蛋白在血管发育过程中各自作用的最新进展。我们专注于现有的体内和体外模型和已知的人类疾病表型，并强调 DOCK 蛋白功能障碍在血管疾病发病机制中的潜在机制。