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• W2602593172 abstract "ABSTRACT Tubulointerstitial fibrosis (TIF) is recognized as a final phenotypic manifestation in the transition from chronic kidney disease (CKD) to end-stage renal disease (ESRD). Here we show that conditional inactivation of Sav1 in the mouse renal epithelium resulted in upregulated expression of profibrotic genes and TIF. Loss of Sav1 induced Stat3 activation and a senescence-associated secretory phenotype (SASP) that coincided with the development of tubulointerstitial fibrosis. Treatment of mice with the YAP inhibitor verteporfin (VP) inhibited activation of genes associated with senescence, SASPs, and activation of Stat3 as well as impeded the development of fibrosis. Collectively, our studies offer novel insights into molecular events that are linked to fibrosis development from Sav1 loss and implicate VP as a potential pharmacological inhibitor to treat patients at risk for developing CKD and TIF." @default.
• W2602593172 created "2017-04-07" @default.
• W2602593172 creator A5021611287 @default.
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• W2602593172 date "2017-06-01" @default.
• W2602593172 modified "2023-09-24" @default.
• W2602593172 title "<i>Sav1</i> Loss Induces Senescence and Stat3 Activation Coinciding with Tubulointerstitial Fibrosis" @default.
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• W2602593172 doi "https://doi.org/10.1128/mcb.00565-16" @default.
• W2602593172 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/5452723" @default.
• W2602593172 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/28320873" @default.
• W2602593172 hasPublicationYear "2017" @default.
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