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All rights reserved. http://resource.belframework.org/belframework/20131211/knowledge/large_corpus.bel http://purl.org/dc/elements/1.1/title BEL Framework Large Corpus Document http://resource.belframework.org/belframework/20131211/knowledge/large_corpus.bel http://purl.org/pav/authoredBy http://www.tkuhn.ch/bel2nanopub/RAqfIUaDiYDM8CsXp_qQLci7X0wGZ5KwRqEsf4TuEZRUI#_6 http://resource.belframework.org/belframework/20131211/knowledge/large_corpus.bel http://purl.org/pav/version 20131211 http://www.tkuhn.ch/bel2nanopub/RAqfIUaDiYDM8CsXp_qQLci7X0wGZ5KwRqEsf4TuEZRUI#_5 http://www.w3.org/ns/prov#value Angiotensin II (Ang II) participates in the pathogenesis of cardiovascular diseases. In hypertension, Ang II via AT1 receptors induces vascular structural changes, including cell hypertrophy, accumulation of extracellular matrix (ECM) proteins, and induction of profibrotic growth factors, such as connective tissue growth factor (CTGF).3 This growth factor also mediates cell proliferation/apoptosis, migration, cellular adhesion, wound healing, and angiogenesis.4 CTGF overexpression has been found in human atherosclerotic and myocardial lesions as well as in the aorta of Ang II–infused rats, associated with ECM accumulation. In VSMCs, CTGF acts as a downstream mediator of Ang II–induced fibrosis. The AT1 are G-coupled receptors that activate several intracellular signaling systems, such as protein kinases (MAPK and Rho kinase [ROCK]), small G proteins, including Ras, Rac1 and RhoA, transcription factors (AP-1, Smads), and redox process, which regulate several Ang II–mediated responses. In VSMCs, statins inhibited Ang II-induced Rho membrane localization and activation. 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