ArticleJournal of the American Society of Nephrology : JASN2020
Tubule-Specific Mst1/2 Deficiency Induces CKD
Article in Journal of the American Society of Nephrology : JASN, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.
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36 citing papers in PubMed, 51 citations in OpenAlex.
- Constitutive YAP activation in distal nephron segments disrupts epithelial identity and nephron patterning.JCI insight · 2026Article
- Targeting the lncRNA PVT-1-Hippo signaling axis in kidney diseases: an emerging therapeutic paradigm.Molecular biology reports · 2026Review
- GADD45B promotes apoptosis in intestinal ischemia/reperfusion through DNA demethylation of MST1/Hippo.Chinese medical journal · 2026Article
- Sialic Acids in Kidney Disease: Immune Regulation, Complement Activation and Glomerular Injury.Antioxidants (Basel, Switzerland) · 2026Review
- 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
- iPSC-based drug discovery identified the Hippo signaling pathway as a therapeutic target in the fibrosis of NPHP1-deficient nephronophthisis.Stem cell research & therapy · 2025Article
- MST3 Regulates AMPK and YAP-Hippo Signaling in Cell Models Relevant to Renal Fibrosis.Biomolecules & therapeutics · 2025Article
- The EZH2 selective inhibitor ZLD1039 attenuates UUO-induced renal fibrosis by suppressing YAP activation.Molecular biomedicine · 2025Article
- Ferulic acid lipid nano capsules versus its native form in alleviating diabetic nephropathy induced in rats through TGF-β1/Hippo pathway crosstalk modulation.Scientific reports · 2025Article
- The Hippo Pathway in Kidney Development.Encyclopedia · 2025Article
- 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
- Variants in tubule epithelial regulatory elements mediate most heritable differences in human kidney function.Nature genetics · 2024Article
- Targeting Neuraminidase 4 Attenuates Kidney Fibrosis in Mice.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- Review
- Novel Protein Biomarkers and Therapeutic Targets for Type 1 Diabetes and Its Complications: Insights from Summary-Data-Based Mendelian Randomization and Colocalization Analysis.Pharmaceuticals (Basel, Switzerland) · 2024Article
- Activation of the YAP/KLF5 transcriptional cascade in renal tubular cells aggravates kidney injury.Molecular therapy : the journal of the American Society of Gene Therapy · 2024Article
- Retinoic acid induced specific changes in the phosphoproteome of C17.2 neural stem cells.Journal of cellular and molecular medicine · 2024Article
- Article
- Inactivation of MST1/2 Controls Macrophage Polarization to Affect Macrophage-Related Disease via YAP and Non-YAP Mechanisms.International journal of biological sciences · 2024Article
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Authors and funding
13 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundThe serine/threonine kinases MST1 and MST2 are core components of the Hippo pathway, which has been found to be critically involved in embryonic kidney development. Yes-associated protein (YAP) and transcriptional coactivator with PDZ-binding motif (TAZ) are the pathway's main effectors. However, the biologic functions of the Hippo/YAP pathway in adult kidneys are not well understood, and the functional role of MST1 and MST2 in the kidney has not been studied.
methodsWe used immunohistochemistry to examine expression in mouse kidneys of MST1 and MST2, homologs of Hippo in
resultsMST1 and MST2 were predominantly expressed in the tubular epithelial cells of adult kidneys. Deletion of Mst1/Mst2 in renal tubules increased activity of YAP but not TAZ. The kidneys of mutant mice showed progressive inflammation, tubular and glomerular damage, fibrosis, and functional impairment; these phenotypes were largely rescued by deletion of Yap in renal tubules. TNF-
conclusionsOur findings show that tubular Mst1/Mst2 deficiency leads to CKD through both the YAP and non-YAP pathways and that tubular YAP activation induces renal fibrosis. The pathogenesis seems to involve the reciprocal stimulation of TNF-
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