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MS-Final-revised.pdf
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Final Accepted Manuscript
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Univ Arizona, Dept Basic Med Sci, Coll Med PhoenixIssue Date
2020-05-16
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ELSEVIERCitation
AlQudah, M., Hale, T. M., & Czubryt, M. P. (2020). Targeting the renin-angiotensin-aldosterone system in fibrosis. Matrix Biology, 91, 92-108.Journal
MATRIX BIOLOGYRights
Copyright © 2020 Elsevier B.V. All rights reserved.Collection Information
This item from the UA Faculty Publications collection is made available by the University of Arizona with support from the University of Arizona Libraries. If you have questions, please contact us at repository@u.library.arizona.edu.Abstract
Fibrosis is characterized by excessive deposition of extracellular matrix components such as collagen in tis-sues or organs. Fibrosis can develop in the heart, kidneys, liver, skin or any other body organ in response to injury or maladaptive reparative processes, reducing overall function and leading eventually to organ failure. A variety of cellular and molecular signaling mechanisms are involved in the pathogenesis of fibrosis. The renin-angiotensin-aldosterone system (RAAS) interacts with the potent Transforming Growth Factor beta (TGF beta) pro-fibrotic pathway to mediate fibrosis in many cell and tissue types. RAAS consists of both classical and alternative pathways, which act to potentiate or antagonize fibrotic signaling mechanisms, respectively. This review provides an overview of recent literature describing the roles of RAAS in the pathogenesis of fibrosis, particularly in the liver, heart, kidney and skin, and with a focus on RAAS interactions with TGF beta sig-naling. Targeting RAAS to combat fibrosis represents a promising therapeutic approach, particularly given the lack of strategies for treating fibrosis as its own entity, thus animal and clinical studies to examine the impact of natural and synthetic substances to alter RAAS signaling as a means to treat fibrosis are reviewed as well. (c) 2020 Elsevier B.V. All rights reserved.Note
12 month embargo; published online 16 May 2020ISSN
0945-053XEISSN
1569-1802PubMed ID
32422329Version
Final accepted manuscriptae974a485f413a2113503eed53cd6c53
10.1016/j.matbio.2020.04.005
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