ArticleNature communications2022
Loss of CLDN5 in podocytes deregulates WIF1 to activate WNT signaling and contributes to kidney disease.
Article in Nature communications, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers, 1 of them a synthesis that pooled it.
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Who cites it
29 citing papers in PubMed, 1 synthesis or guideline pooled it, 39 citations in OpenAlex.
- Approach to Studies on Podocyte Lesions Mediated by Hyperglycemia: A Systematic Review.International journal of molecular sciences · 2025Pooled it
- Molecular mechanisms and novel therapeutic targets of diabetic kidney disease.Chinese medical journal · 2026Review
- Cell-cell crosstalk in kidney health and disease.Nature reviews. Nephrology · 2026Review
- From Endothelial Barrier Dysfunction to Circulating Biomarker: Clinical Potential of Claudin-5 in Thoracic Aortic Aneurysm and Dissection.Journal of clinical medicine · 2026Article
- Lipid metabolism drives podocyte injury in diabetic kidney disease.Frontiers in immunology · 2026Review
- Claudin 5 Across the Vascular Landscape: From Blood-Tissue Barrier Regulation to Disease Mechanisms.Cells · 2025Review
- Claudin Proteins: Their Potential Role in Obesity and Adipose Tissue Signaling, Physiology and Disease.Nutrients · 2025Review
- PRDM16 deficiency promotes podocyte injury by impairing insulin receptor signaling.Cell death and differentiation · 2025Article
- Adipocyte CLDN5 promotes thermogenesis and energy expenditure through regulation of IL10 expression.Nature communications · 2025Article
- Novel Insights into Emx2 and Dmrta2 Cooperation during Cortex Development and Evidence for Dmrta2 Function in the Choroid Plexus.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2025Article
- Inhibition of SIRT1/HSF1 pathway contributes to doxorubicin-induced nephrotoxicity in ovarian tumor-bearing mice.Apoptosis : an international journal on programmed cell death · 2025Article
- Mechanisms of Acute Kidney Injury-Chronic Kidney Disease Transition: Unraveling Maladaptive Repair and Therapeutic Opportunities.Biomolecules · 2025Review
- Wnt signaling in cancer: from biomarkers to targeted therapies and clinical translation.Molecular cancer · 2025Review
- Review
- Key Claudins at the Blood-Retina Barriers.Advances in experimental medicine and biology · 2025Review
- SOX9 regulates epithelial-mesenchymal transformation by mediating the Wnt/Pediatric discovery · 2024Article
- Podocyte cell-specificPhysiological genomics · 2024Article
- LeechWorld journal of gastroenterology · 2024Article
- Podocyte OTUD5 alleviates diabetic kidney disease through deubiquitinating TAK1 and reducing podocyte inflammation and injury.Nature communications · 2024Article
- Tumor Explants Elucidate a Cascade of Paracrine SHH, WNT, and VEGF Signals Driving Pancreatic Cancer Angiosuppression.Cancer discovery · 2024Article
Corrections and comments
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Authors and funding
13 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Although mature podocytes lack tight junctions, tight junction integral membrane protein claudin-5 (CLDN5) is predominantly expressed on plasma membranes of podocytes under normal conditions. Using podocyte-specific Cldn5 knockout mice, we identify CLDN5 as a crucial regulator of podocyte function and reveal that Cldn5 deletion exacerbates podocyte injury and proteinuria in a diabetic nephropathy mouse model. Mechanistically, CLDN5 deletion reduces ZO1 expression and induces nuclear translocation of ZONAB, followed by transcriptional downregulation of WNT inhibitory factor-1 (WIF1) expression, which leads to activation of WNT signaling pathway. Podocyte-derived WIF1 also plays paracrine roles in tubular epithelial cells, as evidenced by the finding that animals with podocyte-specific deletion of Cldn5 or Wif1 have worse kidney fibrosis after unilateral ureteral obstruction than littermate controls. Systemic delivery of WIF1 suppresses the progression of diabetic nephropathy and ureteral obstruction-induced renal fibrosis. These findings establish a function for podocyte CLDN5 in restricting WNT signaling in kidney.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.