ArticleMolecular therapy : the journal of the American Society of Gene Therapy2024
Activation of the YAP/KLF5 transcriptional cascade in renal tubular cells aggravates kidney injury.
Article in Molecular therapy : the journal of the American Society of Gene Therapy, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 14 citations in OpenAlex.
- Article
- Early-activated extracellular matrix proteins shape the metabolic and spatial dynamics of the kidney fibrotic microenvironment.Nature metabolism · 2026Article
- Inhibition of the YAP-E2F2-FGF2 axis in renal tubular cells ameliorates renal fibrosis in chronic kidney disease.Science China. Life sciences · 2026Article
- Multimodal spatial transcriptomic characterization of mouse kidney injury and repair.Nature communications · 2025Article
- Activation of MST1 protects filtration barrier integrity of diabetic kidney disease in mice through restoring the tight junctions of glomerular endothelial cells.Acta pharmacologica Sinica · 2025Article
- Review
- Icariin ameliorates minimal change disease by regulating the mitochondrial dysfunction pathway: an integrated strategy of network pharmacology, bioinformatics, and experimental validation.Frontiers in pharmacology · 2025Article
- Exploring the Functionality of the Krüppel-like Factors in Kidney Development, Metabolism, and Diseases.Life (Basel, Switzerland) · 2024Review
- An improved TEAD dominant-negative protein inhibitor to study Hippo YAP1/TAZ-dependent transcription.bioRxiv : the preprint server for biology · 2024Article
- Interstitial Fluid Shear Stress Induces the Synthetic Phenotype Switching of VSMCs to Release Pro-calcified Extracellular Vesicles via EGFR-MAPK-KLF5 Pathway.International journal of biological sciences · 2024Article
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Authors and funding
12 authors at 6 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The Hippo/YAP pathway plays a critical role in tissue homeostasis. Our previous work demonstrated that renal tubular YAP activation induced by double knockout (dKO) of the upstream Hippo kinases Mst1 and Mst2 promotes tubular injury and renal inflammation under basal conditions. However, the importance of tubular YAP activation remains to be established in injured kidneys in which many other injurious pathways are simultaneously activated. Here, we show that tubular YAP was already activated 6 h after unilateral ureteral obstruction (UUO). Tubular YAP deficiency greatly attenuated tubular cell overproliferation, tubular injury, and renal inflammation induced by UUO or cisplatin. YAP promoted the transcription of the transcription factor KLF5. Consistent with this, the elevated expression of KLF5 and its target genes in Mst1/2 dKO or UUO kidneys was blocked by ablation of Yap in tubular cells. Inhibition of KLF5 prevented tubular cell overproliferation, tubular injury, and renal inflammation in Mst1/2 dKO kidneys. Therefore, our results demonstrate that tubular YAP is a key player in kidney injury. YAP and KLF5 form a transcriptional cascade, where tubular YAP activation induced by kidney injury promotes KLF5 transcription. Activation of this cascade induces tubular cell overproliferation, tubular injury, and renal inflammation.
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