ArticleJournal of the American Society of Nephrology : JASN2013
Wnt4/β-catenin signaling in medullary kidney myofibroblasts.
Article in Journal of the American Society of Nephrology : JASN, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 99 papers.
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Who cites it
99 citing papers in PubMed, 171 citations in OpenAlex.
- Mechanisms of regeneration and maladaptive repair in acute kidney injury.Nature reviews. Nephrology · 2026Review
- Olive Leaf Extract Added to Losartan Treatment Improved Klotho/Wnt/β-Catenin Signaling in Hypertensive Rats with Focal Segmental Glomerulosclerosis.Antioxidants (Basel, Switzerland) · 2026Article
- Sema3dInternational journal of biological sciences · 2026Article
- The kidney stroma in development and disease.Nature reviews. Nephrology · 2025Review
- Mechanisms of Acute Kidney Injury-Chronic Kidney Disease Transition: Unraveling Maladaptive Repair and Therapeutic Opportunities.Biomolecules · 2025Review
- Enhanced reno-protective effects of CHIR99021 modified mesenchymal stem cells against rat acute kidney injury model.BioImpacts : BI · 2025Article
- STAT3 Protein-Protein Interaction Analysis Finds P300 as a Regulator of STAT3 and Histone 3 Lysine 27 Acetylation in Pericytes.Biomedicines · 2024Article
- Wnt Signaling Inhibition Prevents Postnatal Inflammation and Disease Progression in Mouse Congenital Myxomatous Valve Disease.Arteriosclerosis, thrombosis, and vascular biology · 2024Article
- Recent Advances of MSCs in Renal IRI: From Injury to Renal Fibrosis.Bioengineering (Basel, Switzerland) · 2024Review
- SOX9 switch links regeneration to fibrosis at the single-cell level in mammalian kidneys.Science (New York, N.Y.) · 2024Article
- TEA domain transcription factor 1(TEAD1) induces cardiac fibroblasts cells remodeling through BRD4/Wnt4 pathway.Signal transduction and targeted therapy · 2024Article
- Mitochondrial Signaling, the Mechanisms of AKI-to-CKD Transition and Potential Treatment Targets.International journal of molecular sciences · 2024Review
- Cep120 is essential for kidney stromal progenitor cell growth and differentiation.EMBO reports · 2024Article
- Cross-talk of renal cells through WNT signal transduction in the development of fibrotic kidneys.Frontiers in cell and developmental biology · 2024Review
- Cellular cross-talk drives mesenchymal transdifferentiation in diabetic kidney disease.Frontiers in medicine · 2024Review
- Identification of the Main Chemical constituents and mechanism of Renshen Guben oral liquid against Renal Fibrosis.Chinese medicine · 2023Article
- Kidney fibrosis: from mechanisms to therapeutic medicines.Signal transduction and targeted therapy · 2023Review
- ZEB2 controls kidney stromal progenitor differentiation and inhibits abnormal myofibroblast expansion and kidney fibrosis.JCI insight · 2023Article
- Cell derived matrices from bovine corneal endothelial cells as a model to study cellular dysfunction.Experimental eye research · 2023Article
- The Good and the Bad of SHROOM3 in Kidney Development and Disease: A Narrative Review.Canadian journal of kidney health and disease · 2023Review
39 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
5 authors at 5 institutions in 2 countries.
Funding
Abstract
Injury to the adult kidney induces a number of developmental genes thought to regulate repair, including Wnt4. During kidney development, early nephron precursors and medullary stroma both express Wnt4, where it regulates epithelialization and controls smooth muscle fate, respectively. Expression patterns and roles for Wnt4 in the adult kidney, however, remain unclear. In this study, we used reporters, lineage analysis, and conditional knockout or activation of the Wnt/β-catenin pathway to investigate Wnt4 in the adult kidney. Proliferating, medullary, interstitial myofibroblasts strongly expressed Wnt4 during renal fibrosis, whereas tubule epithelia, except for the collecting duct, did not. Exogenous Wnt4 drove myofibroblast differentiation of a pericyte-like cell line, suggesting that Wnt4 might regulate pericyte-to-myofibroblast transition through autocrine signaling. However, conditional deletion of Wnt4 in interstitial cells did not reduce myofibroblast proliferation, cell number, or myofibroblast gene expression during fibrosis. Because the injured kidney expresses multiple Wnt ligands that might compensate for the absence of Wnt4, we generated a mouse model with constitutive activation of canonical Wnt/β-catenin signaling in interstitial pericytes and fibroblasts. Kidneys from these mice exhibited spontaneous myofibroblast differentiation in the absence of injury. Taken together, Wnt4 expression in renal fibrosis defines a population of proliferating medullary myofibroblasts. Although Wnt4 may be dispensable for myofibroblast transformation, canonical Wnt signaling through β-catenin stabilization is sufficient to drive spontaneous myofibroblast differentiation in interstitial pericytes and fibroblasts, emphasizing the importance of this pathway in renal fibrosis.
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Registered trials
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.