血管钙化特别是位于AS斑块内微钙化灶，极易引起斑块破裂，是造成心肌梗死、血管夹层的重要原因；研究提示：NFATc1发挥调控血管钙化的"分子开关"作用。我们前期发现：ApoE-/-小鼠斑块形成中，NFATc1是受CD137-CD137L轴调控斑块进展的下游分子，在斑块早期钙化形成区，NFATc1表达增强，分别激动/抑制该轴，小鼠颈动脉斑块内钙盐沉积增加/减少，NFATc1在平滑肌细胞源性成骨样细胞表达出现上调和下抑。提示：CD137-CD137L轴通过调控NFATc1 启动血管斑块钙化的形成。本研究拟在前期研究基础上探讨NFATc1在CD137-CD137L轴调控斑块钙化形成中作用。以ApoE-/-小鼠和平滑肌细胞为模型，分别过表达和沉默表达NFATc1，验证NFATc1在该轴中承上启下的作用，明确该轴及NFATc1在AS斑块钙化中的作用。阐明该轴通过NFATc1调控AS斑块钙化形成的机制。

Vascular calcification is the main cause of myocardial infarction and vascular dissection, as it can easily result in plaque rupture, especially the microcalcifications in the plaques. It has been prompted that nuclear factor of activated T cells 1 (NFATc1) plays a role as a molecular switch for the regulation of vascular calcification. Our previous studies have demonstrated that NFATc1 is the downstream molecule of CD137-CD137L interaction for the regulation of the development of plaque progression in ApoE-/- mice. In vivo, the expression of NFATc1 in the calcification-forming region of early plaque was significantly upregulated, and excite/inhibit CD137-CD137L interaction respectively, the calcium deposition in the carotid artery plaque in the mice was corresponding increased/decreased. In vitro, the expression of NFATc1 in smooth muscle cell-derived osteoblast-like cells was upregulated/downregulated. These findings suggested that CD137-CD137L interaction can regulate plaque calcification initiated by NFATc1.Therefore, this study is to investigate the effects of NFATc1 on plaque calcification formation regulated by CD137-CD137L interaction on the basis of our previous studies. ApoE-/- mice and smooth muscle cells are used as models, over-expression or silencing-expression of NFATc1 respectively to verify that NFATc1 serves as a connecting link between CD137-CD137L interaction and the calcification of atherosclerotic plaque, and investigate its explicit role of the latter. We aim to clarify the mechanism of CD137-CD137L interaction modulate the expression of NFATc1 to control calcification formation of atherosclerotic plaque.