Studies tend to focus on CCR2+ macrophages infiltrating in the early stage of the injury, while paying less attention to reparative macrophages in the later stage.133 Although numerous findings suggest that there are shared mediators and pathways that regulate inflammation and fibrosis akin to the non-reperfused infarction,7,38 unique mechanisms also make a vast influence on reperfused infarction (Fig. 2d). Here, CCR2 is linked to infarction.