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    Anti-fibrotic Potential of AT(2) Receptor Agonists

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    Author
    Wang, Y; Del Borgo, M; Lee, HW; Baraldi, D; Hirmiz, B; Gaspari, TA; Denton, KM; Aguilar, M-I; Samuel, CS; Widdop, RE
    Date
    2017-08-31
    Source Title
    Frontiers in Pharmacology
    Publisher
    FRONTIERS MEDIA SA
    University of Melbourne Author/s
    Samuel, Chrishan
    Affiliation
    Biochemistry and Molecular Biology
    Metadata
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    Document Type
    Journal Article
    Citations
    Wang, 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 Status
    Open Access
    URI
    http://hdl.handle.net/11343/256915
    DOI
    10.3389/fphar.2017.00564
    Abstract
    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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