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. Author manuscript; available in PMC: 2021 Mar 1.
Published in final edited form as: Semin Nephrol. 2020 Mar;40(2):126–137. doi: 10.1016/j.semnephrol.2020.01.004

Table 1.

Pharmacologic and genetic mediators of Wnt/β-catenin signaling in acute kidney injury.

Pharmacologic Mechanism Effect Ref
DKK-2 Binds to LRP5/6 to enhance binding of Wnt and pathway activation Reduced number of apoptotic tubular epithelial cells in the IRI model of AKI 12
Lithium nhibits GSK3β activity, preventing β-catenin degradation Improved renal morphology, especially in proximal tubules, in cisplatin and IRI models of AKI 35
TDZD-8 Specifically inhibits GSK3β activity, preventing β-catenin degradation Reduced tubular epithelial cell damage and death in the IRI model of AKI 39
Genetic Mechanism Effect Ref
γ-GT-Cre GSK3β Deletion GSK3β ablated specifically in proximal tubular epithelium Reduced apoptosis and mortality in toxin-induced and IRI models of AKI 34
Ksp-Cre β-catenin Deletion β-catenin selectively deleted in tubular epithelium More severe injury and worse mortality in IRI and folic acid models of AKI 36
Gli1-Cre β-catenin Deletion β-catenin selectively deleted in Gli1+fibroblasts Attenuated inflammation and tubular injury in IRI model of AKI 56

Listed in this table are the various compounds and genetic models used to study the role of Wnt/β-catenin signaling in acute kidney injury. In addition, the mechanism of action, the model of injury and the effect on injury are represented. Abbreviations: DKK2, Dickkopf-2; LRP5/6, low density lipoprotein (LDL) receptor related protein 5/6; IRI, ischemia- reperfusion injury; AKI, acute kidney injury; GSK3-β, glycogen synthase kinase 3-β; TDZD-8, thiadiazolidinone 8; γ-GT, gamma-glutamyl transferase; Ksp, kidney-specific cadherin.