In vivo, overexpression of Smad7 attenuates fibrosis in different renal disease models including 5/6 nephrectomy [82], crescentic glomerulonephritis [83], UUO [84], chronic aristolochic acid nephropathy [85], and hypertensive nephropathy [86]. This evidence concerns the gene SMAD7 and crescentic glomerulonephritis.