ArticleKidney international2011
Canonical Wnt/β-catenin signaling mediates transforming growth factor-β1-driven podocyte injury and proteinuria.
Article in Kidney international, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 94 papers.
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Who cites it
94 citing papers in PubMed, 146 citations in OpenAlex.
- Emerging therapeutic pipelines on kidney fibrosis: challenges in translational research.Journal of translational medicine · 2026Review
- Molecular immunopharmacology of traditional Chinese medicine-derived compounds in membranous nephropathy: mechanistic insights into immune aging and kidney essence deficiency.Frontiers in immunology · 2026Review
- Molecular mechanisms in podocytopathies: finding suitable targets for a new era of glomerular gene therapy.Clinical kidney journal · 2026Review
- Glucose metabolic reprogramming in systemic lupus erythematosus and lupus nephritis: theoretical foundations and therapeutic implications.Frontiers in immunology · 2026Review
- Fibroblast activation and heterogeneity in fibrotic disease.Nature reviews. Nephrology · 2025Review
- The Life of a Kidney Podocyte.Acta physiologica (Oxford, England) · 2025Review
- Crosstalk of injured podocytes with parietal epithelial cells through Wnt4/β-Catenin signaling.Scientific reports · 2025Article
- UDA-seq: universal droplet microfluidics-based combinatorial indexing for massive-scale multimodal single-cell sequencing.Nature methods · 2025Article
- Diabetic kidney disease: m6A modification as a marker of disease progression and subtype classification.Frontiers in medicine · 2025Article
- Aging and Intestinal Fibrosis: Mechanisms, Implications, and Therapeutic Strategies.Clinical interventions in aging · 2025Review
- The Pathogenesis of Nephrotic Syndrome: A Perspective from B Cells.Kidney diseases (Basel, Switzerland) · 2024Review
- Matrix metalloproteinases in kidney homeostasis and diseases: an update.American journal of physiology. Renal physiology · 2024Review
- Scutellarin ameliorates diabetic nephropathy via TGF-β1 signaling pathway.Natural products and bioprospecting · 2024Article
- Role of platelet factor 4 in arteriovenous fistula maturation failure: What do we know so far?The journal of vascular access · 2024Review
- Urine MMP7 as a kidney injury biomarker.Clinical kidney journal · 2024Article
- Roles of macrophages in lupus nephritis.Frontiers in pharmacology · 2024Review
- Loss of Dact2 alleviates cisplatin-induced nephrotoxicity through regulation of the Igfl-MAPK pathway axis.Cell biology and toxicology · 2023Article
- Palmitoyltransferase DHHC9 and acyl protein thioesterase APT1 modulate renal fibrosis through regulating β-catenin palmitoylation.Nature communications · 2023Article
- NDUFV1 attenuates renal ischemia-reperfusion injury by improving mitochondrial homeostasis.Journal of cellular and molecular medicine · 2023Article
- TGF-beta signal transduction: biology, function and therapy for diseases.Molecular biomedicine · 2022Review
34 more citing papers are in PubMed but not listed here.
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4 authors at 1 institution in 2 countries.
Funding
Abstract
Transforming growth factor-β1 (TGF-β1) upregulation occurs in virtually all chronic kidney diseases and is associated with podocyte injury and proteinuria; however, the mechanisms contributing to this in vivo are ambiguous. In vitro, incubation of podocytes with TGF-β1 induced Wnt1 expression, β-catenin activation, and stimulated the expression of Wnt/β-catenin downstream target genes. Ectopic expression of Wnt1 or β-catenin mimicked TGF-β1, induced Snail1, and suppressed nephrin expression. The Wnt antagonist, Dickkopf-1, blocked TGF-β1-induced β-catenin activation, Snail1 induction, and nephrin suppression. In vivo, ectopic expression of TGF-β1 induced Wnt1 expression, activated β-catenin, and upregulated Wnt target genes such as Snail1, MMP-7, MMP-9, desmin, Fsp1, and PAI-1 in mouse glomeruli, leading to podocyte injury and albuminuria. Consistently, concomitant expression of Dickkopf-1 gene abolished β-catenin activation, inhibited TGF-β1-triggered Wnt target gene expression, and mitigated albuminuria. Thus, canonical Wnt/β-catenin signaling mediates TGF-β1-driven podocyte injury and proteinuria. These studies suggest that Wnt/β-catenin signaling may be exploited as a therapeutic target for the treatment of proteinuric kidney diseases.
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Registered trials
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