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. 2024 Nov 18;43(6):724–738. doi: 10.23876/j.krcp.23.344

Figure 2. Therapeutic strategies targeting Wnt/β-catenin signaling.

Figure 2.

In the AKI model, β-catenin can be activated and accumulated in cells by Wnt agonist and then transferred to the nucleus. With the involvement of CBP and LEF/TCF, β-catenin increases the transcription of target genes and finally alleviates the early renal function decline and renal structural damage caused by AKI. In the CKD-induced fibrosis model, sclerostin, DKK1 or PPAR-α can competitively bind to LRP5/6, thereby inhibiting β-catenin and its downstream signaling pathways which finally alleviate renal fibrosis. In addition, WIF, Klotho, or sFRP4 can competitively bind to Wnt ligands and frizzled receptors, thereby blocking the binding of Wnt ligands and frizzled receptors and ultimately inhibiting β-catenin and its downstream signaling pathways. Furthermore, ICG-001 competitively binds to CBP, which then inhibits β-catenin mediated gene expression.

AKI, acute kidney injury; CBP, cyclic adenosine monophosphate response-element binding protein; CKD, chronic kidney disease; DKK-1, Dickkopf-1; ICG-001, indirect catenin inhibitor-gamma-001; LEF, lymphoid enhancer binding factor; LRP, lipoprotein receptor protein; PPAR-α, peroxisome proliferator-activated receptor-α; sFRP4, secreted frizzled-related protein 4; TCF, T-cell factor; WIF, Wnt inhibitory factor.