title: The battlefield at arteriovenous crossroads: invading arterial smooth muscle cells occupy the outflow tract of fistulas.
abstract: There is an ongoing debate about the anatomical origin of the neointimal cells that are responsible for venous stenotic lesions in arteriovenous fistulas. Liang and co-workers show that vascular smooth muscle cells from the feeding artery contribute substantially to venous intimal hyperplasia in a murine AVF model. In addition, they show that increased Notch signaling is the driving force behind FSP-1-mediated migration of these cells to the venous outflow tract.
authors: Department of Nephrology, Leiden University Medical Center, Leiden, The Netherlands.|Einthoven Laboratory for Experimental Vascular Medicine, Leiden University Medical Center, Leiden, The Netherlands.
authors: Joris I
authors: JI
authors: Rotmans
authors: Department of Nephrology, Leiden University Medical Center, Leiden, The Netherlands.|Einthoven Laboratory for Experimental Vascular Medicine, Leiden University Medical Center, Leiden, The Netherlands.
authors: Taisiya
authors: T
authors: Bezhaeva
mesh_terms: D000818:Animals; D001166:Arteriovenous Shunt, Surgical / Q000009:adverse effects*; D019917:Blood Vessel Prosthesis Implantation / Q000009:adverse effects*; D002465:Cell Movement; D006083:Graft Occlusion, Vascular / Q000378:metabolism*; D006801:Humans; D008297:Male; D009131:Muscle, Smooth, Vascular / Q000378:metabolism*; D032389:Myocytes, Smooth Muscle / Q000378:metabolism*; D058426:Neointima; D051881:Receptor, Notch1 / Q000378:metabolism*; D051436:Renal Insufficiency, Chronic / Q000628:therapy*
chemical_list: D051881:Receptor, Notch1