CCL2 and glomerulosclerosis: In the current study, the increased systemic and renal MCP-1 and TNF-α expression in db/db mice might have originated from recruited intrarenal macrophages that polarized to M1 and subsequently increased TGF-β- and TNF-α-dependent lymphangiogenesis, which ultimately led to glomerulosclerosis and tubulointerstitial fibrosis.