ArticleKidney international2015
Migration of smooth muscle cells from the arterial anastomosis of arteriovenous fistulas requires Notch activation to form neointima.
Article in Kidney international, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
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Who cites it
32 citing papers in PubMed, 51 citations in OpenAlex.
- RBMS1 Contributes to Early Arteriovenous Fistula Neointimal Remodeling Through Modulation of VSMC Phenotypic Responses.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Vascular Smooth Muscle Cell Metabolic Reprogramming in Arteriovenous Fistula Failure.Biomedicines · 2025Review
- Mineralocorticoid receptor antagonism attenuates arteriovenous fistula stenosis by modulating the phenotype of vascular smooth muscle cells.Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association · 2025Article
- Advancements in Mesenchymal Stem Cell-Based Therapy for Enhancing Arteriovenous Fistula Patency.International journal of molecular sciences · 2024Review
- Review
- Frequent use of percutaneous transluminal angioplasty is not associated with reduced vascular access recreation in a longitudinal ecology study.Scientific reports · 2024Article
- The Pathological Mechanisms and Therapeutic Molecular Targets in Arteriovenous Fistula Dysfunction.International journal of molecular sciences · 2024Review
- The predictive value of systemic immune-inflammation index for vascular access survival in chronic hemodialysis patients.Frontiers in immunology · 2024Article
- The rodent models of arteriovenous fistula.Frontiers in cardiovascular medicine · 2024Review
- Temporal regulation of notch activation improves arteriovenous fistula maturation.Journal of translational medicine · 2022Article
- Localized Perivascular Therapeutic Approaches to Inhibit Venous Neointimal Hyperplasia in Arteriovenous Fistula Access for Hemodialysis Use.Biomolecules · 2022Review
- von Willebrand Factor: A Central Regulator of Arteriovenous Fistula Maturation Through Smooth Muscle Cell Proliferation and Outward Remodeling.Journal of the American Heart Association · 2022Article
- Downregulation of the endothelial histone demethylase JMJD3 is associated with neointimal hyperplasia of arteriovenous fistulas in kidney failure.The Journal of biological chemistry · 2022Article
- Inhibition of β-catenin signaling attenuates arteriovenous fistula thickening in mice by suppressing myofibroblasts.Molecular medicine (Cambridge, Mass.) · 2022Article
- Neutralization of S100A4 induces stabilization of atherosclerotic plaques: role of smooth muscle cells.Cardiovascular research · 2022Article
- Oxidative stress: An essential factor in the process of arteriovenous fistula failure.Frontiers in cardiovascular medicine · 2022Review
- Decreased Jagged1 expression in vascular smooth muscle cells delays endothelial regeneration in arteriovenous graft.Cardiovascular research · 2020Article
- Differences in Transforming Growth Factor-β1/BMP7 Signaling and Venous Fibrosis Contribute to Female Sex Differences in Arteriovenous Fistulas.Journal of the American Heart Association · 2020Article
- Mature Vascular Smooth Muscle Cells, but Not Endothelial Cells, Serve as the Major Cellular Source of Intimal Hyperplasia in Vein Grafts.Arteriosclerosis, thrombosis, and vascular biology · 2020Article
- Role of Hypoxia and Metabolism in the Development of Neointimal Hyperplasia in Arteriovenous Fistulas.International journal of molecular sciences · 2019Review
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7 authors at 2 institutions in 2 countries.
Funding
Abstract
A major factor contributing to failure of arteriovenous fistulas (AVFs) is migration of smooth muscle cells into the forming neointima. To identify the source of smooth muscle cells in neointima, we created end-to-end AVFs by anastomosing the common carotid artery to the jugular vein and studied neural crest-derived smooth muscle cells from the carotid artery, which are Wnt1-positive during development. In Wnt1-cre-GFP mice, smooth muscle cells in the carotid artery but not the jugular vein are labeled with GFP. About half of the cells were GFP-positive in the neointima, indicating their migration from the carotid artery to the jugular vein in AVFs created in these mice. As fibroblast-specific protein-1 (FSP-1) regulates smooth muscle cell migration, we examined FSP-1 in failed AVFs and polytetrafluoroethylene grafts from patients with end-stage kidney disease or from AVFs in mice with chronic kidney disease. In smooth muscle cells of AVFs or polytetrafluoroethylene grafts, FSP-1 and activation of Notch1 are present. In smooth muscle cells, Notch1 increased RBP-Jκ transcription factor activity and RBP-Jκ stimulated FSP-1 expression. Conditional knockout of RBP-Jκ in smooth muscle cells or general knockout of FSP-1 suppressed neointima formation in AVFs in mice. Thus, the artery of AVFs is the major source of smooth muscle cells during neointima formation. Knockout of RBP-Jκ or FSP-1 ameliorates neointima formation and might improve AVF patency during long-term follow-up.
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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.