Previous studies have shown that ET-1 can activate NF-κB, MAPK, and other signaling pathways, leading to mesangial matrix expansion, glomerulosclerosis, and podocyte injury (89)ET-1 induces a series of pathophysiological changes by binding to the ETA receptor (ETAR) and ETB receptor (ETBR) (90). This evidence concerns the gene EDN1 and glomerulosclerosis.