血管发育始于胚胎早期的血管发生，该过程受到多层面、高度整合的分子网络调控，其中转录后调控机制仍有待系统解析。细胞质多聚腺苷酸结合蛋白1a (cytoplasmic poly(A) binding protein 1a，Pabpc1a)是一种关键的RNA结合蛋白，通过转录后调控参与多种生理与病理过程，但其在血管发育中的功能仍不清楚。本研究首先发现pabpc1a在血管发生的关键时间窗口于内皮细胞中表达，随后利用CRISPR/Cas9技术构建了pabpc1a基因缺失模型。功能实验表明，pabpc1a基因缺失导致动静脉特化相关基因表达失调，动静脉血管直径比例异常；而过表达pabpc1a可以有效挽救血管发生缺陷。机制上，组学分析显示pabpc1a基因缺失引起内皮细胞中广泛的基因表达紊乱，其中翻译、核糖体生物合成及能量代谢相关通路显著下调。这些结果提示，Pabpc1a可能通过协调蛋白质合成与代谢稳态来确保血管发生的正常进行。综上所述，本研究证明Pabpc1a是血管发生过程中一个不可或缺的转录后调节因子，为理解血管发育的调控网络提供了新视角。

Vascular development begins with vasculogenesis during early embryogenesis. This process is controlled by a highly integrated, multi-layered molecular network. However, the role of post-transcriptional regulation in this context remains poorly understood. Cytoplasmic poly(A) binding protein 1a (Pabpc1a) is a key RNA-binding protein that regulates gene expression at the post-transcriptional level and participates in many physiological and pathological processes. Its role in vascular development, however, is still unclear. In this study, we first found that pabpc1a is highly expressed in endothelial cells during the critical window of vasculogenesis. We then generated a pabpc1a knockout model using CRISPR/Cas9. Functional analyses showed that loss of pabpc1a disrupted the expression of genes involved in arterial-venous specification and altered the arterial-to-venous diameter ratio. In contrast, overexpression of pabpc1a effectively rescued the vascular defects. Mechanistically, transcriptomic analysis revealed widespread gene expression changes in endothelial cells lacking pabpc1a. Pathways related to translation, ribosome biogenesis, and energy metabolism were significantly downregulated. These findings suggest that Pabpc1a regulates vasculogenesis by coordinating protein synthesis and metabolic homeostasis. In summary, our study demonstrates Pabpc1a as an essential post-transcriptional regulator during vasculogenesis and provides new insight into the regulatory network governing vascular development.