ArticleKidney international2015
The battlefield at arteriovenous crossroads: invading arterial smooth muscle cells occupy the outflow tract of fistulas.
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 4 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
4 citing papers in PubMed.
- Temporal regulation of notch activation improves arteriovenous fistula maturation.Journal of translational medicine · 2022Article
- Arteriovenous conduits for hemodialysis: how to better modulate the pathophysiological vascular response to optimize vascular access durability.American journal of physiology. Renal physiology · 2019Review
- Deficiency of TLR4 homologue RP105 aggravates outward remodeling in a murine model of arteriovenous fistula failure.Scientific reports · 2017Article
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2 authors.
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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.
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Registered trials
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