无水乙醇栓塞颅面部动静脉畸形疗法已展示良好应用前景，而巨大、复杂动静脉畸形难以彻底治愈，残存病变极易进展。内皮细胞生物学行为异常是其重要原因。既往研究发现BMP10通路传导障碍可致内皮细胞生物学行为异常；miR-18a可稳定内皮细胞正常生物学行为。本课题组研究发现栓塞后残存病变进展与BMP10通路传导受损有关，且该通路调控因子Smurf1为miR-18a的潜在调控靶点。据此推测：栓塞后miR-18a修复受损BMP10通路，影响内皮细胞生物学行为，进而抑制或减缓残存病变进展。本项目拟以猪动静脉畸形模型为载体，结合细胞分子生物学及影像学等方法，在申请人前期研究无水乙醇栓塞动静脉畸形基础上，围绕栓塞后残存病变进展这一核心问题，阐明miR-18a对BMP10通路的影响，探索miR-18a调控残存病变内皮细胞生物学行为的新机制。这些基础性探索有望为抑制或减缓残存病变进展提供新思路，具有重要理论意义。

Absolute ethanol embolization of craniofacial arteriovenous malformations (AVMs) has shown good application prospects, however, huge and complex AVMs are difficult to cure. Residual lesions are easy to progress. The abnormal biological behavior of endothelial cells is an important reason. Previous studies have found that the dysfunction of BMP10 pathway conduction could lead to abnormal biological behavior of endothelial cells, and miR-18a could stabilize the normal biological behavior of endothelial cells. Our study found that the progress of residual lesions after embolization is related to the impairment of BMP10 pathway, and the regulation factor Smurf1 is a potential target of miR-18a. Above all, we suggest that the effect of the repair of the damaged BMP10 pathway by miR-18a on the progression of residual lesions after embolization. This study intends to employ pig AVMs model, molecular biology and imageology and other methods, based on previous study of ethanol embolization of arteriovenous malformation and around the key issue of residual lesions progression after embolization, to elucidate the effect of miR-18a on the BMP10 pathway and explore the new mechanism of miR-18a regulating the endothelial cell biological behavior of residual lesions. These basic exploration is expected to provide new ideas for inhibiting or slowing down the progress of residual lesions.