Evidence for the combined involvement of heparanase, TGF-β and ET-1 in the fibrosis/inflammatory response to AKI is provided by showing that treatment with PG545 prior to I/R maintained a normal epithelial phenotype and abolished the EMT transcriptional program exemplified by a marked decrease in the levels of VIM, FN, α-SMA, IL-6, ET-1 and TGF-β. The gene discussed is FN1; the disease is acute kidney injury.