探讨急性冠脉综合征（acute coronary syndrome，ACS）病程中易损斑块的发生机制并寻找有效的干预靶点，已成为心血管研究领域中亟待解决的重要课题之一。在本课题组的前期研究中发现血清淀粉样蛋白A（serum amyloid A，SAA）血清水平的升高不仅是机体处于动脉粥样硬化（atherosclerosis，AS）慢性炎症状态的体现，更直接加速了AS斑块的形成。然而SAA在AS易损斑块形成过程中所发挥的作用及其机制国内外尚未见报道。本课题组通过构建SAA-/-ApoE-/-双敲小鼠及慢病毒转染SAA过表达ApoE-/-小鼠，揭示SAA对斑块稳定性的影响，围绕其受体FPRL1、基质金属蛋白酶、胶原等调控斑块稳定性的关键因子，探讨血清SAA对AS斑块稳定性的影响；同时在体外实验中对其作用机制及相关信号转导通路进行深入研究，旨在为ACS的防治提供新的干预靶点和实验依据。

Acute coronary syndrome (ACS), mostly triggered by the ruptured atherosclerotic plaque, is responsible for the high mortality worldwide, and thus becomes a hot topic in the field of cardiovascular research. In our previous studies, we have already found that serum amyloid A (SAA) is not only a biomarker of chronic status in atherosclerosis, but also a critical mediator in accelerating the progression of AS directly. However, the potential role of SAA in the pathogenesis of vulnerable plaque has not been reported yet. The animal model of SAA-/-ApoE-/- double-knocked mice and over-expressed ApoE-/- mice by murine SAA lentivirus intravenous injection was established to reveal the influence on the stability of vulnerable plaque. Focusing on the key regulatory factors such as matrix metalloproteinases (MMPs), collagen and its receptor(FPRL1), the influence of SAA on plaque vulnerability will be elucidated. Meanwhile, the relative signaling pathway involved in this process will be investigated in vitro. Our rearch will provide a new theoretical support on understanding the pathological mechanism of atherosclerotic plaque vulnerability and may be helpful in designing a novel therapeutic target against ACS.