In this study, we demonstrate that (1) Bone marrow-derived fibroblasts express CCR2; (2) CCR2 deficiency inhibits bone marrow-derived fibroblast accumulation and macrophage infiltration in the kidneys in response to obstructive injury; (3) CCR2 deficiency inhibits MCP-1 and CXCL16 gene expression; (4) CCR2 deficiency suppresses the transformation of bone marrow-derived myofibroblast and the expression of α-SMA and FSP-1; (5) CCR2 deficiency reduces renal fibrosis and the expression of ECM proteins. The gene discussed is CCL2; the disease is renal fibrosis.