研究[41]发现,在DDP引起的AKI中,许多炎症因子包括IL-1β、IL-6、IL-18、单核细胞趋化蛋白-1(monocyte chemotactic protein-1, MCP-1)、调节活化正常T细胞表达与分泌的趋化因子(regulated upon activation normal T cell expressed and secreted, RANTES)、巨噬细胞炎症蛋白-2(macrophage inflammatory protein-2, MIP-2)、细胞间粘附分子-1(intercellular cell adhesion molecule-1, ICAM-1)、转化生长因子-β(transforming growth factor beta, TGF-β)表达增多。但在小鼠中抑制IL-1、IL-6及IL-18后,AKI的发生并未减少。. This evidence concerns the gene CCL2 and acute kidney injury.