MCP-1 is released after kidney injury, prompting the recruitment of CCR2-positive monocytes/macrophages, dendritic cells, and fibroblasts to the injury site after binding to CCR2 and promotes the progression of kidney inflammation and fibrosis (Fig. 2).[2,38,44–46] The MCP-1/CCR2 axis does not directly mediate polarization of pro-fibrotic macrophages. Here, CCL2 is linked to nephritis.