▪Significant inhibition of UUO-induced collagen-1 and TIF▪Reduction of thrombin-activated PAR-1 expression in the fibrotic kidney▪Improved histoarchitecture of the obstructed kidney▪Inhibited TGF-β and SNAI2-induced epithelial-mesenchymal transition (EMT)In summary, dabigatran was found to be effective in inhibiting renal injury and fibrosis in a mouse model. It significantly reduced markers associated with inflammation and fibrosis, suggesting its potential as a therapeutic agent for chronic kidney disease, particularly in conditions involving tubulointerstitial fibrosis. This evidence concerns the gene TGFB1 and chronic kidney disease.