Matches in SemOpenAlex for { <https://semopenalex.org/work/W3023647415> ?p ?o ?g. }
- W3023647415 abstract "The Wnt/β-catenin signaling pathway plays an important role in renal development and is reexpressed in the injured kidney and other organs. β-Catenin signaling is protective in acute kidney injury (AKI) through actions on the proximal tubule, but the current dogma is that Wnt/β-catenin signaling promotes fibrosis and development of chronic kidney disease (CKD). As the role of proximal tubular β-catenin signaling in CKD remains unclear, we genetically stabilized (i.e., activated) β-catenin specifically in murine proximal tubules. Mice with increased tubular β-catenin signaling were protected in 2 murine models of AKI to CKD progression. Oxidative stress, a common feature of CKD, reduced the conventional T cell factor/lymphoid enhancer factor-dependent β-catenin signaling and augmented FoxO3-dependent activity in proximal tubule cells in vitro and in vivo. The protective effect of proximal tubular β-catenin in renal injury required the presence of FoxO3 in vivo. Furthermore, we identified cystathionine γ-lyase as a potentially novel transcriptional target of β-catenin/FoxO3 interactions in the proximal tubule. Thus, our studies overturned the conventional dogma about β-catenin signaling and CKD by showing a protective effect of proximal tubule β-catenin in CKD and identified a potentially new transcriptional target of β-catenin/FoxO3 signaling that has therapeutic potential for CKD." @default.
- W3023647415 created "2020-05-13" @default.
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- W3023647415 date "2020-05-21" @default.
- W3023647415 modified "2023-10-10" @default.
- W3023647415 title "Tubular β-catenin and FoxO3 interactions protect in chronic kidney disease" @default.
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- W3023647415 doi "https://doi.org/10.1172/jci.insight.135454" @default.
- W3023647415 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/7259539" @default.
- W3023647415 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/32369448" @default.
- W3023647415 hasPublicationYear "2020" @default.
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