The battlefield at arteriovenous crossroads: invading arterial smooth muscle cells occupy the outflow tract of fistulas.
other · Level V
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- Record sourced from PubMed, PMID 26323067.
- Also identified by DOI 10.1038/ki.2015.124.
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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.
Medical subject headings
- Arteriovenous Shunt, Surgical
- Blood Vessel Prosthesis Implantation
- Cell Movement
- Graft Occlusion, Vascular
- Muscle, Smooth, Vascular
- Myocytes, Smooth Muscle
- Neointima
- Receptor, Notch1
- Renal Insufficiency, Chronic