AGK（酰基甘油激酶）最初被鉴定为一种线粒体跨膜蛋白，具有脂质激酶功能。最近的研究确定了AGK促进肿瘤生长和转移，增强CD8+ T细胞的糖酵解代谢和功能适应性，或调节巨核细胞分化的作用。然而，AGK在血小板活化和动脉血栓形成中的作用仍需阐明。我们使用自动血液分析仪进行了血液学分析，并通过透射电镜研究了血小板形态。我们利用转基因小鼠，体外血小板功能实验和体内血栓形成模型探索了AGK在血小板活化和动脉血栓形成中的作用。我们通过共免疫沉淀、质谱、免疫荧光和Western blot揭示了AGK对Talin-1的调节作用。同时，我们使用特定的ELISA试剂盒测试了AGK对磷脂酸/裂解磷脂酸的脂质合成和凝血酶生成的作用。在本研究中，我们发现AGK缺乏或AGK突变对血小板平均体积、血小板微结构或主要血小板膜受体的表达水平均没有影响。然而，AGK缺乏或AGK突变显著降低血小板活化的多个方面，包括诱导剂诱导的血小板聚集、颗粒分泌、JON /A结合、Fg（纤维蛋白原）上的扩展和凝块收缩。AGK缺乏或AGK突变还明显延迟了动脉血栓形成，但对尾部出血时间和血小板促凝功能没有影响。机制研究揭示了AGK通过促进Talin-1Ser425的磷酸化以及影响αIIbβ3介导的双向信号通路来增强血小板活化和动脉血栓形成。然而，AGK不影响血小板中裂解磷脂酸/裂解磷脂酸的脂质合成。

AGK (acylglycerol kinase) was first identified as a mitochondrial transmembrane protein that exhibits a lipid kinase function. Recent studies have established that AGK promotes cancer growth and metastasis, enhances glycolytic metabolism and function fitness of CD8+ T cells, or regulates megakaryocyte differentiation. However, the role of AGK in platelet activation and arterial thrombosis remains to be elaborated.We performed hematologic analysis using automated hematology analyzer and investigated platelets morphology by transmission electron microscope. We explored the role of AGK in platelet activation and arterial thrombosis utilizing transgenic mice, platelet functional experiments in vitro, and thrombosis models in vivo. We revealed the regulation effect of AGK on Talin-1 by coimmunoprecipitation, mass spectrometry, immunofluorescence, and Western blot. We tested the role of AGK on lipid synthesis of phosphatidic acid/lysophosphatidic acid and thrombin generation by specific Elisa kits.In this study, we found that AGK depletion or AGK mutation had no effect on the platelet average volumes, the platelet microstructures, or the expression levels of the major platelet membrane receptors. However, AGK deficiency or AGK mutation conspicuously decreased multiple aspects of platelet activation, including agonists-induced platelet aggregation, granules secretion, JON/A binding, spreading on Fg (fibrinogen), and clot retraction. AGK deficiency or AGK mutation also obviously delayed arterial thrombus formation but had no effect on tail bleeding time and platelet procoagulant function. Mechanistic investigation revealed that AGK may promote Talin-1Ser425 phosphorylation and affect the αIIbβ3-mediated bidirectional signaling pathway. However, AGK does not affect lipid synthesis of lysophosphatidic acid/lysophosphatidic acid in platelets.AGK, through its kinase activity, potentiates platelet activation and arterial thrombosis by promoting Talin-1 Ser425 phosphorylation and affecting the αIIbβ3-mediated bidirectional signaling pathway.