CCL2 and renal fibrosis: Cheng et al. also reported that IS could upregulate the phosphorylation of signal transducers and activators of transcription-3 (STAT-3), subsequently increasing the production of TGF-β1, MCP-1/CCL2, and α-SMA, which molecular changes are implicated in stromal inflammation, renal fibrosis, and further CKD progression [19].