动脉粥样硬化（AS）斑块内血管新生是造成斑块内出血及破裂的重要促发因素，CD137信号是参与AS进展的关键分子。我们前期发现：CD137信号促进AS斑块形成，诱导斑块内血管新生；ApoE-/-小鼠斑块内存在CD31（内皮细胞）和CD68（巨噬细胞）免疫荧光共定位。体外实验显示内皮细胞与巨噬细胞共培养时，CD137信号促进血管新生能力明显增强，并且激活CD137信号能够促发巨噬细胞发生极性漂移。因此，我们提出如下假说：CD137信号通过调控巨噬细胞极性漂移介导斑块内血管新生。本研究在前期基础上，以CD137信号调控巨噬细胞极性漂移启动血管新生为主线，在动物、细胞模型及在体微环境基础上，分别激动和抑制CD137信号，观察该信号对巨噬细胞极性漂移及血管新生的影响，明确CD137信号如何调控巨噬细胞极性漂移，阐明其调控巨噬细胞极性漂移介导血管新生机制。该研究有望为AS易损斑块防治带来新的契机。

Angiogenesis is an important factor in atherosclerotic plaques which contributing to intraplaque hemorrhage and plaque rupture. CD137 signal is a key molecule involved in the progression of atherosclerosis . Our previous study found that CD137 signal promoted atherosclerotic plaque formation and induced angiogenesis in plaques. Animal experiments show that CD31 (endothelial cell markers) are immunofluorescence co-located with CD68 (macrophage markers) in the plaques of ApoE-/- mice. The ability of angiogenesis induced by CD137 signal is remarkably enhanced when the endothelial cells are co-cultured with macrophages in vitro. Activation of CD137 signal also promotes macrophage polarization drift. In summary, we put forward the following hypothesis: CD137 signal induces angiogenesis in atherosclerotic plaques by regulating macrophage polarization drift. Based on our previous work, we focus on the effect of CD137 signaling on angiogenesis which regulated by macrophage polarization drift. CD137 signal is activated or inhibited in vivo/vitro and microenvironment, respectively. The effects of CD137 signal on macrophage polarization drift and angiogenesis were observed. We aim to reveal the potential mechanism of macrophage polarization drift inducing angiogenesis regulated by CD137 signal. Our study may present a novel therapeutic strategy against the unstable plaque.