ArticleMolecular medicine (Cambridge, Mass.)2022
Inhibition of β-catenin signaling attenuates arteriovenous fistula thickening in mice by suppressing myofibroblasts.
Article in Molecular medicine (Cambridge, Mass.), 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 10 citations in OpenAlex.
- A Vein Attempt? Experimental Models for Arteriovenous Fistula Research.Cardiovascular engineering and technology · 2026Review
- Human Data First: New Biological Premises for Arteriovenous Fistula Research.Arteriosclerosis, thrombosis, and vascular biology · 2026Review
- Evaluating Animal Models for Improved Hemodialysis Vascular Access: A Focus on Arteriovenous Fistula.Medical science monitor : international medical journal of experimental and clinical research · 2025Review
- Article
- Advancements in Mesenchymal Stem Cell-Based Therapy for Enhancing Arteriovenous Fistula Patency.International journal of molecular sciences · 2024Review
- Albendazole ameliorates aerobic glycolysis in myofibroblasts to reverse pulmonary fibrosis.Journal of translational medicine · 2024Article
- The Pathological Mechanisms and Therapeutic Molecular Targets in Arteriovenous Fistula Dysfunction.International journal of molecular sciences · 2024Review
- Exploring the role of ITGB6: fibrosis, cancer, and other diseases.Apoptosis : an international journal on programmed cell death · 2024Review
- Disturbed flow in the juxta-anastomotic area of an arteriovenous fistula correlates with endothelial loss, acute thrombus formation, and neointimal hyperplasia.American journal of physiology. Heart and circulatory physiology · 2024Article
- TGF-β1, pSmad-2/3, Smad-7, and β-Catenin Are Augmented in the Pulmonary Arteries from Patients with Idiopathic Pulmonary Fibrosis (IPF): Role in Driving Endothelial-to-Mesenchymal Transition (EndMT).Journal of clinical medicine · 2024Article
- Pyrvinium Pamoate: Past, Present, and Future as an Anti-Cancer Drug.Biomedicines · 2022Review
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Authors and funding
12 authors at 5 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundArteriovenous fistula (AVF) is the most important vascular access for hemodialysis; however, preventive treatment to maintain the patency of AVFs has not been developed. In endothelium, β-catenin functions in both the intercellular adherens complex and signaling pathways that induce the transition of endothelial cells to myofibroblasts in response to mechanical stimuli. We hypothesize that mechanical disturbances in the AVF activate β-catenin signaling leading to the transition of endothelial cells to myofibroblasts, which cause AVF thickening. The present study aimed to test this hypothesis.
methodsChronic kidney disease in mice was induced by a 0.2% adenine diet. AVFs were created by aortocaval puncture. Human umbilical vein endothelial cells (HUVECs) were used in the cell experiments. A pressure-culture system was used to simulate mechanical disturbances of the AVF.
resultsCo-expression of CD31 and smooth muscle alpha-actin (αSMA), loss of cell-cell adhesions, and the expression of the myofibroblast marker, integrin subunit β6 (ITGB6), indicated transition to myofibroblasts in mouse AVF. Nuclear translocation of β-catenin, decreased axin2, and increased c-myc expression were also observed in the AVF, indicating activated β-catenin signaling. To confirm that β-catenin signaling contributes to AVF lesions, β-catenin signaling was inhibited with pyrvinium pamoate; β-catenin inhibition significantly attenuated AVF thickening and decreased myofibroblasts. In HUVECs, barometric pressure-induced nuclear localization of β-catenin and increased expression of the myofibroblast markers, αSMA and ITGB6. These changes were attenuated via pretreatment with β-catenin inhibition.
conclusionsThe results of this study indicate that mechanical disturbance in AVF activates β-catenin signaling to induce the transition of endothelial cells to myofibroblasts. This signaling cascade can be targeted to maintain AVF patency.
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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.