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. 2008 Dec 17;3(12):e3959. doi: 10.1371/journal.pone.0003959

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Rodríguez-Vita et al.

This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are properly credited.

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Proposed model for statin interaction with the TGF-β/Smad pathway in atherosclerosis. In normal conditions TRII and TGF-β expression is regulated by RhoA through ROCK activation. Hyperactivation of RhoA in pathological condition may lead to the downregulation of TRII and TGF-β that characterizes unstable plaques. Statins inhibit prenylation of RhoA, thus increasing TRII expression and TGF- β release. The TRII upregulation allows TGF-β present in serum or induced by statins to activate the Smad pathway and increase ECM proteins production. These effects may promote plaque stability.