文献报道APJ受体内源性配体apelin-13促血管平滑肌细胞（VSMC）迁移参与动脉粥样硬化，铁自噬与细胞迁移及高尔基体应激（GAS）密切相关，而神经元钙传感器1（NCS1）可调控GAS，且存在豆蔻酰化修饰位点。预实验发现apelin-13促VSMC豆蔻酰转移酶（NMT1）和NCS1表达，诱导GAS和铁自噬，据此提出“NMT1豆蔻酰化NCS1促进GAS诱导铁自噬介导apelin-13/APJ促VSMC迁移”科学假说，课题拟采用慢病毒转染等技术，明确apelin-13是否促NCS1豆蔻酰化、GAS及铁自噬；阐明豆蔻酰化NCS1促GAS是否介导apelin-13诱导VSMC铁自噬；分析豆蔻酰化NCS1促GAS诱导铁自噬是否介导apelin-13促VSMC迁移。课题以豆蔻酰化NCS1-GAS-铁自噬新视角揭示apelin-13促VSMC迁移新机理，为VSMC迁移性疾病的APJ药物研发提供依据。

Previous article reported that APJ endogenous ligand apelin-13 promotes the migration of vascular smooth muscle cells (VSMC) involved in atherosclerosis, and ferritinophagy is closely related to cell migration and Golgi Apparatus Stress(GAS), and neuronal calcium sensor 1 (NCS1) regulates GAS, and NCS1 has a myristoylation modification site. Preliminary experiments identified that apelin-13 promoted the expression of VSMC N-myristoyltransferase (NMT1) and neuronal calcium sensor 1 (NCS1), induced GAS and ferritinophagy. Accordingly, we proposed the hypothesis that "apelin-13 through NMT1 myristoylation NCS1 promotion GAS induced ferritinophagy to promote migration of vascular smooth muscle cell”. Thus, we intend to use CO-IP、lentiviral transfection technology and other assays to identify whether apelin-13 induces NMT1, NCS1 myristoylation, promotes GAS, and induces ferritinophagy; and to clarify whether apelin-13 promotes NCS1 myristoylation and induces GAS；Clarify whether myristoylated NCS1 promotes GAS-mediated apelin-13-induced VSMC ferritinophagy；To analyze whether NMT1 myristoylation of NCS1 promotes GAS-induced ferritinophagy mediates apelin-13-induced VSMC migration. From the new perspective that NMT1 myristoylation of NCS1 promotes GAS-induced ferritinophagy, we can clarify a new mechanism apelin-13 promotes VSMC migration, and provides a theoretical basis for the development of APJ drugs for VSMC-associated migration diseases.