动脉粥样硬化（AS）是心血管疾病致残致死的主要原因。及时干预早期动脉粥样硬化（EAS），可使AS维持稳定，甚至消退。在体检测EAS的标准尚未确立，其进展机制及调控方式并不清楚，目前尚无病理学证实的联合FD-OCT/NIRS检测EAS的研究。巨噬细胞与AS发展关系密切，而内质网应激（ERS）可调控巨噬细胞功能，有研究表明CTRP9可通过AMPK通路抑制ERS。调控巨噬细胞功能可能是干预EAS进展的关键环节。于是我们提出假说：CTRP9可通过干预ERS影响巨噬细胞功能调控EAS发生发展。本项目拟在动物模型中确定与病理学吻合的EAS腔内影像学诊断标准和生物标志物变化规律，探究ERS（在相应的调控条件下）、巨噬细胞功能与EAS的关系，并应用FD-OCT/NIRS及生物标志物动态观察EAS变化。本项目可为临床诊断EAS提供确定的标准，探索防控EAS进展的靶点，为干预EAS建立一定的科学基础。

Coronary artery atherosclerosis is the leading cause of morbidity and mortality in cardiovascular diseases. Timely intervening early atherosclerosis (EAS) can make it degenerate into stable lesions even be regressed. How to detect EAS and prevent its progression remains unclear. There is no research on combining FD-OCT and NIRS to detect EAS verified by pathology. Endoplasmic reticulum stress (ERS) , as an important factor, modulates macrophage function promoting the initiation and progression of atherosclerosis. Therefore, regulating ERS in macrophage may be a potential strategy in intervening EAS. Studies have shown that C1q/TNF-related proteins 9 (CTRP9) can inhibit ERS through AMPK pathway. So we hypothesize thatCTRP9 can intervene the progression of EAS through regulating macrophage function via inhibiting ERS. Our study aims to establish the intravascular imaging diagnostic criteria, define novel relevant biomarkers, clarify the mechanism of macrophage function regulated by CTRP9 in vitro, and furthermore dynamic evaluate the effect of CTRP9 on EAS by combing FD-OCT/NIRS and biomarkers in vivo.