In addition, fibrosis was reduced, suggesting that under the same circumstances of renal injury, kidney inflammation and fibrosis were alleviated in MCP-1 knockout mice.[62] Sakata et al also showed that high sodium chloride intake could downregulate the expression of MCP-1 in 5/6 nephrectomized mice, recruit macrophages to the damaged kidney, and aggravate the progression of renal fibrosis.[38] The studies indicate that inflammation plays a key role in renal fibrosis. This evidence concerns the gene CCL2 and nephritis.