In addition, endostatin- overexpressing transgenic mice revealed renal tubulointerstitial fibrosis at a younger age, with increased circulating endostatin and accelerated renal dysfunction and fibrosis in folic acid-induced nephropathy [86], suggesting that the process by which endostatin is generated from type XVIII collagen in the kidney is likely to contribute to the pathogenesis of renal fibrosis. Here, COL18A1 is linked to renal fibrosis.