阻塞性睡眠呼吸暂停（OSA）特点是慢性间歇性低氧（IH）, 是血脂异常与动脉粥样硬化的危险因素。但慢性IH诱发血脂异常和动脉粥样硬化的机制尚不清楚，我们推测脂蛋白脂酶（LPL）抑制剂血管生成素样蛋白4（Angptl4）及炎症介质白三烯B4（LTB4）通路在其中具有重要作用。本项目通过建立和使用体外和体内慢性IH诱发血脂异常及动脉粥样硬化的模型，使用药物和基因敲除的方法，研究脂肪Angptl4 及 LTB4 通路在慢性IH诱发血脂异常和动脉粥样硬化中的作用及调控机制，进一步阐明慢性IH诱发血脂异常和动脉粥样硬化的机制，期望为OSA相关的动脉粥样硬化性心血管疾病的治疗提供可能的新的靶点。

Obstructive sleep apnea (OSA) is characterized by chronic intermittent hypoxia (IH), which is a risk factor for dyslipidemia and atherosclerosis. The mechanisms by which chronic IH induces dyslipidemia and atherosclerosis are unclear. We speculate that lipoprotein lipase (LPL) inhibitor, angiopoietin-like protein 4 (Angptl4), and inflammatory mediators leukotriene B4 (LTB4) in which the pathway play an important role. We use both in vitro and in vivo chronic IH models, and explore the adipose Angptl4 and LTB4 pathway contribution to dyslipidemia and atherogenesis using both pharmacologic and genetic approaches. We hope to further clarify the mechanisms of IH-induced dyslipidemia and atherosclerosis, and provide a potential novel therapeutic target for obstructive sleep apnea-associated atherosclerotic cardiovascular disease.