Anti-fibrotic Potential of AT(2) Receptor Agonists
Web of Science
AuthorWang, Y; Del Borgo, M; Lee, HW; Baraldi, D; Hirmiz, B; Gaspari, TA; Denton, KM; Aguilar, M-I; Samuel, CS; Widdop, RE
Source TitleFrontiers in Pharmacology
PublisherFRONTIERS MEDIA SA
University of Melbourne Author/sSamuel, Chrishan
AffiliationBiochemistry and Molecular Biology
Document TypeJournal Article
CitationsWang, Y., Del Borgo, M., Lee, H. W., Baraldi, D., Hirmiz, B., Gaspari, T. A., Denton, K. M., Aguilar, M. -I., Samuel, C. S. & Widdop, R. E. (2017). Anti-fibrotic Potential of AT(2) Receptor Agonists. FRONTIERS IN PHARMACOLOGY, 8 (AUG), https://doi.org/10.3389/fphar.2017.00564.
Access StatusOpen Access
There are a number of therapeutic targets to treat organ fibrosis that are under investigation in preclinical models. There is increasing evidence that stimulation of the angiotensin II type 2 receptor (AT2R) is a novel anti-fibrotic strategy and we have reviewed the published in vivo preclinical data relating to the effects of compound 21 (C21), which is the only nonpeptide AT2R agonist that is currently available for use in chronic preclinical studies. In particular, the differential influence of AT2R on extracellular matrix status in various preclinical fibrotic models is discussed. Collectively, these studies demonstrate that pharmacological AT2R stimulation using C21 decreases organ fibrosis, which has been most studied in the setting of cardiovascular and renal disease. In addition, AT2R-mediated anti-inflammatory effects may contribute to the beneficial AT2R-mediated anti-fibrotic effects seen in preclinical models.
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