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- Ivan G Gomez, Monica Grafals, Didier Portilla, and Jeremy S Duffield.
- Division of Nephrology, Seattle, WA, USA. igomez@uw.edu
- J Formos Med Assoc. 2013 May 1; 112 (5): 237243237-43.
AbstractOne cornerstone of chronic kidney disease (CKD) is fibrosis, as kidneys are susceptible due to their high vascularity and predisposition to ischemia. Presently, only therapies targeting the angiotensin receptor are used in clinical practice to retard the progression of CKD. Thus, there is a pressing need for new therapies designed to treat the damaged kidney. Several independent laboratories have identified a number of microRNAs that are dysregulated in human and animal models of CKD. This review will explore the evidence suggesting that by blocking the activity of such dysregulated microRNAs, new therapeutics could be developed to treat the progression of CKD.Copyright © 2013. Published by Elsevier B.V.
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