Pharmacological modulation of epithelial mesenchymal transition caused by angiotensin II. Role of ROCK and MAPK pathways.

Purpose Tubulointerstitial fibrosis is a final common pathway to end-stage chronic kidney diseases, which are characterized by elevated renal angiotensin II (AngII) production. This peptide participates in kidney damage inducing fibrosis and epithelial mesenchymal transition (EMT). Our aim was to describe potential therapeutic targets in AngII-induced EMT, investigating the blockade of different intracellular pathways.