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Studies in renal fibrosis have shown that liraglutide inhibited the activation of downstream classical and non-canonical signaling pathways (p-Smad3 and p-ERK1/2) by reducing the expression of TGF-β1 and its receptors, thereby inhibiting TGF-β1-induced epithelial–mesenchymal transition (EMT) in NRK-52E cells, which effectively prevented the fibrosis process in chronic kidney disease [13]
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