ArticleKidney international2017
Podocyte-specific JAK2 overexpression worsens diabetic kidney disease in mice.
Article in Kidney international, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 64 papers, 2 of them syntheses that pooled it.
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Who cites it
64 citing papers in PubMed, 2 syntheses or guidelines pooled it, 93 citations in OpenAlex.
- Optimizing diabetic kidney disease animal models: Insights from a meta-analytic approach.Animal models and experimental medicine · 2023Pooled it
- A systematic review and meta-analysis of cell-based interventions in experimental diabetic kidney disease.Stem cells translational medicine · 2021Pooled it
- JAK1/JAK2 inhibition by baricitinib in diabetic kidney disease: results from a Phase 2 randomized controlled clinical trial.Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association · 2018Trial
- Targeting cellular senescence in diabetic kidney disease: potential of regenerative, cell-based therapies and other senotherapeutic approaches.Kidney international · 2026Review
- Lipids in kidney diseases: from systemic imbalance to intrarenal alterations of cellular lipid metabolism in rare and common kidney diseases.Journal of molecular medicine (Berlin, Germany) · 2026Review
- JAK3 Staining and CD68+ Macrophage Counts Are Increased in Patients with IgA Nephropathy.Diagnostics (Basel, Switzerland) · 2026Article
- Intra-Leukemic Interferon Signaling Suppresses Expansion and Mediates Chemoresistance in Human AML.Blood cancer discovery · 2026Article
- Article
- Mechanistic Insights into Antioxidant Interventions Targeting Obesity-Induced Oxidative Stress in the Pathogenesis and Complications of Type 2 Diabetes Mellitus.Current issues in molecular biology · 2025Review
- Inflammation in cardiovascular-kidney-metabolic syndrome: key roles and underlying mechanisms-a comprehensive review.Molecular and cellular biochemistry · 2025Review
- Single-Cell RNA Sequencing Delineates Renal Anti-Fibrotic Mechanisms Mediated by TRPC6 Inhibition.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Epigenetic associations with kidney disease in individuals of African ancestry with APOL1 high-risk genotypes and HIV.Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association · 2025Article
- Comprehending the Role of Metabolic and Hemodynamic Factors Alongside Different Signaling Pathways in the Pathogenesis of Diabetic Nephropathy.International journal of molecular sciences · 2025Review
- The Noncanonical Wnt5a-CaJournal of cellular and molecular medicine · 2025Article
- Identification of Ferroptosis-related Genes for Diabetic Nephropathy by Bioinformatics and Experimental Validation.Current pharmaceutical design · 2025Article
- Inflammation in glomerular diseases.Frontiers in immunology · 2025Review
- Identification and Validation of Tryptophan Metabolism-Related Genes in Diabetic Kidney Disease and Construction of a Clinical Prediction Model.Journal of diabetes research · 2025Article
- Crosstalk between ferroptosis and innate immune in diabetic kidney disease: mechanisms and therapeutic implications.Frontiers in immunology · 2025Review
- Alterations in the Levels of Urinary Exosomal MicroRNA-183-5p and MicroRNA-125a-5p in Individuals with Type 2 Diabetes Mellitus.Biomedicines · 2024Article
- Type 2 diabetes mellitus in adults: pathogenesis, prevention and therapy.Signal transduction and targeted therapy · 2024 · on this mapReview
4 more citing papers are in PubMed but not listed here.
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Authors and funding
10 authors at 1 institution in 1 country.
Funding
Abstract
Activation of JAK-STAT signaling has been implicated in the pathogenesis of diabetic kidney disease. An increased expression of JAK-STAT genes was found in kidney glomerular cells, including podocytes, in patients with early diabetic kidney disease. However, it is not known whether increased expression of JAK or STAT isoforms in glomerular cells can lead to worsening nephropathy in the setting of diabetes. Therefore, we overexpressed JAK2 mRNA specifically in glomerular podocytes of 129S6 mice to determine whether this change alone could worsen diabetic kidney disease. A 2-3 fold increase in glomerular JAK2 expression, an increase similar to that found in humans with early diabetic kidney disease, led to substantial and statistically significant increases in albuminuria, mesangial expansion, glomerulosclerosis, glomerular fibronectin accumulation, and glomerular basement membrane thickening, and a significant reduction in podocyte density in diabetic mice. Treatment with a specific JAK1/2 inhibitor for 2 weeks partly reversed the major phenotypic changes of diabetic kidney disease and specifically normalized expression of a number of downstream STAT3-dependent genes implicated in diabetic kidney disease progression. Thus, moderate increases in podocyte JAK2 expression at levels similar to those in patients with early diabetic kidney disease can lead directly to phenotypic and other alterations of progressive diabetic glomerulopathy. Hence, inhibition of these changes by treatment with a JAK1/2 inhibitor suggests that such treatment may help retard progression of early diabetic kidney disease in patients.
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