| Literature DB >> 31017009 |
Stephanie L K Bowers1,2, Stephanie Davis-Rodriguez1,2,3, Zachary M Thomas1,2, Valeria Rudomanova1,2, W Clark Bacon1,2, Alex Beiersdorfer1,2, Qing Ma1,3, Prasad Devarajan1,3, Burns C Blaxall1,2.
Abstract
Fibrosis is a common feature of chronic kidney disease; however, no clinical therapies effectively target the progression of fibrosis. Inhibition of fibronectin polymerization with the small peptide pUR4 attenuates fibrosis in the liver and heart. Here, we show that pUR4 decreases renal fibrosis and tissue remodeling using a clinically relevant model of kidney injury, unilateral ischemia-reperfusion. This work highlights the benefits of inhibiting matrix polymerization, alone or in conjunction with cell-based therapies, as a novel approach to diminish the maladaptive responses to ischemic kidney injury that lead to chronic renal failure.Entities:
Keywords: acute kidney injury; chronic kidney disease; fibronectin; fibrosis; ischemia-reperfusion
Mesh:
Substances:
Year: 2019 PMID: 31017009 PMCID: PMC6620592 DOI: 10.1152/ajprenal.00117.2019
Source DB: PubMed Journal: Am J Physiol Renal Physiol ISSN: 1522-1466