The present study was undertaken to investigate whether interstitial fibrosis could be prevented by abolishing TSP-1 function in unilateral ureteral obstruction (UUO)-induced renal fibrosis.
These results show that constitutively active PKG inhibits the fibrogenic potential of high glucose through repression of TSP1-dependent TGF-beta bioactivity, suggesting that gene transfer of the catalytic domain of PKG might provide a new strategy for treatment of diabetic renal fibrosis.