冠状动脉慢性闭塞（CTO）病变是冠状动脉粥样硬化的一种复杂类型，其临床发病率高、预后差。因此，探索CTO病变特异性干预手段具有非常重要的临床意义。组织病理学证实巨噬细胞和成纤维细胞是CTO病变中两种主要细胞成分，二者交互作用所促发的炎症级联反应在CTO病理过程中发挥重要作用，但具体机制尚不明确。我们前期工作和国内外研究发现KCa3.1通道通过调控JAK/STAT和TGF-β/Smad信号途径分别在巨噬细胞和成纤维细胞活化和表型转化中发挥关键作用，是调控二者交互作用的共同信号分子。由此提示，KCa3.1通道可作为CTO病变形成过程中分子层面的干预靶点。本课题将从分子、细胞和整体动物三个层面以及正、反两个方向对KCa3.1通道介导巨噬细胞和成纤维细胞交互作用在CTO病变发生发展中的作用进行深入研究，为临床防治CTO病变提供新思路。

Coronary chronic total occlusion (CTO)，a complicated form of coronary atherosclerosis, is characterized by high morbidity prognosis. Therefore, investigation of specific interventions for the treatment of CTO is of great clinical importance. Macrophages and fibroblasts were confirmed to be two major component cells of CTO. Inflammatory cascade mediated by the cross-talk between macrophages and fibroblasts plays an important role in the pathogenesis of CTO. However, the detailed mechanism is still unclear. Our previous work and results reported by other studies showed that KCa3.1 channels regulating JAK/STAT and TGF-β/Smad pathway play crucial role in the activation and phenotype polarization of macrophages and fibroblasts respectively, and KCa3.1 channel could be a common signal transducer of the cross-talk between macrophages and fibroblasts. These findings indicate that KCa3.1 channel is a potential therapeutic target for CTO. In this project, we will investigate KCa3.1 channel-mediated cross-talk between fibroblasts and macrophages in the pathogenesis of coronary chronic total occlusion and its molecular mechanism from various levels and direction, which may provide an alternative strategy for the prevention and treatment of CTO.