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This study investigated the differences of angiogenesis in cirrhotic and non-cirrhotic PHT with special emphasis on the canonical (Shh\/Gli) and non-canonical (Shh\/RhoA) hedgehog pathway. Cirrhotic (bile duct ligation\/BDL; CCl<jats:sub>4<\/jats:sub> intoxication) and non-cirrhotic (partial portal vein ligation\/PPVL) rats received either atorvastatin (15\u2009mg\/kg; 7d) or control chow before sacrifice. Invasive hemodynamic measurement and Matrigel implantation assessed angiogenesis <jats:italic>in vivo<\/jats:italic>. Angiogenesis <jats:italic>in vitro<\/jats:italic> was analysed using migration and tube formation assay. In liver and vessel samples from animals and humans, transcript expression was analyzed using RT-PCR and protein expression using Western blot. Atorvastatin decreased portal pressure, shunt flow and angiogenesis in cirrhosis, whereas atorvastatin increased these parameters in PPVL rats. Non-canonical Hh was upregulated in experimental and human liver cirrhosis and was blunted by atorvastatin. Moreover, atorvastatin blocked the non-canonical Hh-pathway RhoA dependently in activated hepatic steallate cells (HSCs). Interestingly, hepatic and extrahepatic Hh-pathway was enhanced in PPVL rats, which resulted in increased angiogenesis. In summary, <jats:italic>s<\/jats:italic>tatins caused contrary effects in cirrhotic and non-cirrhotic portal hypertension. Atorvastatin inhibited the non-canonical Hh-pathway and angiogenesis in cirrhosis. 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