Table 1. Possible role of Hippo pathway component activation in AKI.
Component | Model | Species | Effect | Role | References |
AKI: Acute kidney injury; I/R injury: Ischemia-reperfusion injury; AA: Aristolochic acid; UA: Uranyl acetate; UUO: Unilateral ureter obstructive. | |||||
MST1 | I/R injury | Mouse | MST1 up-regulation accelerates progression of AKI via activation of mitochondrial fission. | Detrimental | Li et al., 2019 |
I/R injury | Mouse | Genetic ablation of MST1 attenuates tubular epithelia apoptosis and kidney injury by repressing mitochondrial fission. | Detrimental | Feng et al., 2018a | |
SAV1 | UUO | Mouse | SAV1 depletion in RTECs exhibits aggravated renal TIF. | Protective | Seo et al., 2016 |
AA | Mouse | SAV1 loss results in up-regulated expression of profibrotic genes and TIF. | Protective | Leung et al., 2017 | |
TAZ | I/R injury | Mouse | TAZ expression ameliorates tubular injury and reduces apoptosis in kidney after I/R injury. | Protective | Wu et al., 2020 |
AA | Mouse | TAZ is activated in fibrosis through TGF-β1-dependent mechanisms and sustained TAZ signaling promotes epithelial maladaptive repair. | Protective | Anorga et al., 2018 | |
YAP | UA | Rat | Transient overexpression of YAP in renal epithelia recovered from AKI inhibits apoptosis and results in acquired cytoresistance. | Protective | Iwakura et al., 2017 |
I/R injury | Mouse | YAP activation after AKI mediates renal epithelial cell regeneration. | Protective | Chen et al., 2018 | |
I/R injury | Rat | Transient YAP activation may promote repair of injured epithelia. Constant YAP activation may lead to interstitial fibrosis and abnormal renal tubule differentiation. |
Transient: Protective Persistent: Detrimental |
Xu et al., 2016 | |
I/R injury | Mouse | YAP activation in post-acute phase of AKI is implicated in renal dysfunction and TIF. | Persistent: Detrimental |
Xu et al., 2021 | |
I/R injury | Mouse | Tubular YAP persistent activation is associated with maladaptive repair and interstitial macrophage infiltration. | Persistent: Detrimental |
Zheng et al., 2021 | |
YAP/TAZ | I/R injury/UUO | Mouse | YAP/TAZ activation promotes macrophage M2 polarization and contributes to kidney fibrosis. | Detrimental | Feng et al., 2018b |
UUO | Mouse | YAP/TAZ knockout suppresses UUO-induced ECM deposition, myofibroblast accumulation and TIF. | Detrimental | Liang et al., 2017 |