脂蛋白a是动脉粥样硬化形成与进展的高危因素，脂蛋白a大小和浓度由apo(a)决定。apo(a)具有激活巨噬细胞释放炎症介质的作用，可能通过下调巨噬细胞自噬导致动脉粥样硬化斑块不稳定，参与冠心病发生发展。apo(a)由LPA基因编码，遗传率高达0.68-0.98。我们前期研究发现，LPA基因rs10455872和rs3798220变异可能是影响脂蛋白a浓度的重要靶点。我们拟进一步探讨LPA基因变异与广西壮族人冠心病发生与预后的关系。研究包括：1. 分析LPA基因rs10455872和rs3798220变异与广西壮族人脂蛋白a、冠心病易感性、左室射血分数、心血管终点事件的关系。2. 观察LPA基因杂合子和纯合子供体apo(a)对THP-1巨噬细胞自噬基因Beclin-1和LC3-II表达及自噬体形成的影响，并通过使用PI3K-Akt-mTOR通路抑制剂，探讨apo(a)下调巨噬细胞自噬的机制。

Lipoprotein a is an independent risk factor of atherosclerosis. The size and concentration levels of lipoprotein a are decided by apo(a). Apo(a) strongly stimulating macrophages to release inflammatory factors may down regulate the autophagy of macrophages, which may be an important factor for the instability of atherosclerotic plaque inducing coronary artery disease. Apo(a) is encoded by LPA gene and is under strong genetic control (heritability=0.68–0.98). Our preliminary study highly indicated that variations of LPA gene rs10455872 and rs3798220 may be the important targets involving in the regulation of peripheral blood lipoprotein a concentration. We will further investigate the correlation between the two polymorphisms of LPA gene and coronary artery disease in Guangxi Zhuang population. The present study includes two parts: Part 1. The correlation analysis of LPA gene rs10455872 and rs3798220 variations with the susceptibility to coronary artery disease, left ventricular ejection fraction and cardiovascular events in Guangxi Zhuang population. Part 2. Discussion on different expression levels of autophagy gene Beclin-1 and LC3-II in human THP-1 derived macrophages in different conditions such as LPA gene heterozygote and homozygote donors derived different apo(a) and the possible mechanism of down-regulation of autophagy of human THP-1 derived macrophages through PI3K-Akt-mTOR pathway.