MCP-1, a chemokine upregulated by hyperglycemia, advanced glycation end-products, and oxidative stress, recruits monocytes/macrophages to renal tissue and drives tubulointerstitial inflammation and fibrosis through CCR2-mediated signaling, thereby contributing to albuminuria, glomerulosclerosis, and functional decline [37,38]. This evidence concerns the gene CCL2 and glomerulosclerosis.