ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2024
Meis1 Targets Protein Tyrosine Phosphatase Receptor J in Fibroblast to Retard Chronic Kidney Disease Progression.
Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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The trial behind it
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Who cites it
9 citing papers in PubMed.
- Quercetin Alleviates Ferroptosis-Induced Renal Fibrosis by Modulating the PRDM9/HMOX1/PTGS2 Axis.ACS omega · 2026Article
- The role of classical protein tyrosine phosphatases in diabetic kidney disease and therapeutic implications.Journal of biomedical science · 2026Review
- Meis1-driven suppression of MIF/CD74 signaling promotes M2 macrophage polarization and protects against inflammatory damage in experimental acute lung injury.Cell biology and toxicology · 2026Article
- Dysregulation of the Upb1-3-ureidopropionate Pathway Impairs Fatty Acid Metabolism and Exacerbates Acute Kidney Injury.International journal of biological sciences · 2026Article
- HOX and MEINOX in cellular plasticity, fibrosis, and cancer.World journal of stem cells · 2025Review
- In Situ Assembly of Fluorogenic RNA for Screening Natural Anti-Liver Fibrosis Products via Dynamic Visualization of COL1A1 mRNA.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Histone methylation modification and diabetic kidney disease: Potential molecular mechanisms and therapeutic approaches (Review).International journal of molecular medicine · 2024Review
- Meis1 Targets Protein Tyrosine Phosphatase Receptor J in Fibroblast to Retard Chronic Kidney Disease Progression.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- Enhanced miR-214 in Vascular Endothelial Cells Retards Renal Inflammation and Glomerular Sclerosis in Five-Sixths Nephrectomy Mice.Kidney diseases (Basel, Switzerland)Article
Corrections and comments
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Authors and funding
13 authors.
Funding
Abstract
Renal fibrosis is a common pathological feature of chronic kidney disease (CKD) with the proliferation and activation of myofibroblasts being definite effectors and drivers. Here, increased expression of Meis1 (myeloid ecotropic viral integration site 1) is observed, predominantly in the nucleus of the kidney of CKD patients and mice, and negatively correlates with serum creatinine. Fibroblast-specific knock-in of Meis1 inhibits myofibroblast activation and attenuates renal fibrosis and kidney dysfunction in CKD models. Overexpression of Meis1 in NRK-49F cells suppresses the pro-fibrotic response induced by transforming growth factor-β1 but accelerates by its knockdown. Mechanistically, Meis1 targets protein tyrosine phosphatase receptor J (Ptprj) to block renal fibrosis by inhibiting the proliferation and activation of fibroblasts. Finally, a new activator of Ptprj is identified through computer-aided virtual screening, which has the effect of alleviating renal fibrosis. Collectively, these results illustrate that the Meis1/Ptprj axis has therapeutic potential for clinically treating CKD.
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Registered trials
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