https://www.selleckchem.com/pr....oducts/l-dehydroasco
The epithelial-mesenchymal transition (EMT) is usually considered the central mechanism of podocyte injury that eventually leads to proteinuria. We used an in vitro TGF-β1 induced podocyte EMT model and an in vivo rat focal segmental glomerulosclerosis (FSGS) model to uncover the mechanism underlying the protective effect of triptolide (TP) on podocytes. We found that TP could reverse the podocyte EMT process and upregulate the expression of TET2 in the TGF-β1-induced podocyte injury model. Bisulfite amplicon sequencing (
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