炎症是心肌梗死（MI）的关键机制，而且是心肌损伤与抗损伤中复杂的平衡过程。巨噬细胞在MI进展中具有重要作用，但机制有待进一步阐明。我们前期研究发现阻断CXCR6/CXCL16信号通路减少CD11b+单核细胞向损伤心肌组织的迁移，抑制心肌细胞自噬而发挥心肌保护作用。我们近期研究揭示急性MI促进CD11b+Gr-1+细胞动员和浸润心肌组织，加重心肌损伤，硫化氢（hydrogen sulfide, H2S）可调控免疫细胞、抑制炎症反应，发挥心肌保护作用。假说：H2S和CXCR6/CXCL16信号通路可介导急性MI后巨噬细胞的动员及分化，调控炎症，减轻心肌损伤。本项目拟采用野生型和CXCR6-KO小鼠建立急性MI模型，从分子、细胞到动物，阐明H2S-CXCR6/CXCL16信号通路在急性MI后巨噬细胞动员、分化（M1/M2）、心肌损伤和心室重构中的作用，希望可以为临床急性MI患者的治疗提供新靶向。

Inflammatory processes is critical for MI and underlie a complicated balance in myocardial infarction and protection. Macrophages are an important contributor to the pathophysiology of cardiac injury and pertaining to pathological mechanisms are an evolving area of intense research and debate. However, the mechanisms of macrophage in acute MI remain further data accumulate. Our previous study found that the CD11b+ monocytes were significantly inhibited and the autophagy was attenuated contributing to acute MI via disruption of the CXCL16/CXCR6 signaling cascade. In addition, our preliminary experiments investigated the cardioprotective effects of H2S were enhanced by inhibiting the migration of CD11b+Gr-1+ myeloid cells from the spleen into the blood and by attenuating post-infarction inflammation. Therefore, we put forward the hypothesis that H2S and CXCR6/CXCL16 signaling pathway play important roles in the proliferation, activation, and differentiation of macrophages, contributing to regulate the immune cells, suppress the inflammation of acute MI, and protect the myocardial ischemia injury. To prove the hypothesis, we will construct acute MI murine models with wild type and CXCR6-KO mice. We want to investigate the mechanisms of H2S-CXCR6/CXCL16 signaling pathway in the activation and differentiation (M1/M2) of macrophages associated to acute MI and cardiac fibrosis, and try to shed light on the novel targets of fundamental study and clinic therapy of acute MI.