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Statins, Rho GTPases and KLF2: new mechanistic insight into liver fibrosis and portal hypertension
  1. Jonel Trebicka,
  2. Robert Schierwagen
  1. Department of Internal Medicine I, University of Bonn, Bonn, Germany
  1. Correspondence to Dr Jonel Trebicka, Department of Internal Medicine I, University of Bonn, Sigmund-Freud-Str. 25, Bonn 53127, Germany; Jonel.trebicka{at}ukb.uni-bonn.de

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Statins, standard of care drugs used in metabolic syndrome and cardiovascular diseases, seem to be safe for chronic liver disease.1 ,2 Beyond their cholesterol-lowering effect by inhibition of 3-hydroxy-3-methyl-glutaryl-CoA reductase (HMG-CoA reductase), statins exert multiple pleiotropic effects.3 These pleiotropic effects make statins cheap and also well-investigated drugs in terms of tolerability and safety. Therefore, statins offer possibilities not only to test new hypotheses, and reveal novel pathomechanisms and targets, as shown by Marrone et al in this issue,4 but also for therapeutic approaches. Indeed, use of statins might attenuate liver fibrosis in patients with chronic hepatitis C infection;5 it reduced hepatic vascular resistance and portal pressure in patients with cirrhosis.6 ,7 The Barcelona group has performed pioneer clinical and experimental work for the use of statins in portal hypertension. A recent Spanish multicentre study, headed by the same group and presented in European Association for the Study of the Liver (EASL) 2014, showed that statins …

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