Inhibition of the Wnt/β-catenin signaling pathway reduces autophagy levels in complement treated podocytes

xlomafota13 shared this article with you from Inoreader Inhibition of the Wnt/β-catenin signaling pathway reduces autophagy levels in complement treated podocytes Via Experimental and therapeutic medicine Exp Ther Med. 2021 Jul;22(1):737. doi: 10.3892/etm.2021.10169. Epub 2021 May 9. ABSTRACT In idiopathic membranous nephropathy, the complement membrane attack complex, more commonly referred to as complement 5b-9 (C5b-9), induces glomerular epithelial cell injury and proteinuria. C5b-9 can also activate numerous mechanisms that restrict or facilitate injury. Recent studies suggest that autophagy and the canonical Wnt signaling pathway serve an important role in repairing podocyte injury. However, the effect of C5b-9 on these pathways and the relationship between them remains unclear. The aim of the present study was to show the effect of C5b-9 on the Wnt/β-catenin signaling pathway and autophagy in podocytes in vitro. Levels of relevant indicators were detected by immunofluorescence staining and capillary western immunoassay. C5b-9 serum significantly activated the Wnt/β-catenin signaling pathway and promoted autophagy. Treatme nt with Dickkopf-related protein 1 (DKK1), a Wnt/β-catenin pathway blocker, protected podocytes from injury and significantly inhibited autophagy. The results indicated that inhibition of the Wnt/β-catenin pathway physiologically activated autophagy. The results indicated that C5b-9 resulted in a decrease in Akt in podocytes. However, the podocytes preincubated with DKK1 and then attacked by C5b-9 showed an increase in Akt levels. This may explain the observation that blocking the Wnt/β-catenin signaling pathway attenuated C5b-9 podocyte damage, while inhibiting autophagy. The results of the present study also suggest that regulation of these two pathways may serve as a novel method for the treatment of idiopathic membranous nephropathy. PMID:34055054 | PMC:PMC8138266 | DOI:10.3892/etm.2021.10169 View on the web Inoreader. Take back control of your news feed. Follow us on Twitter and Facebook.