ArticleScientific reports2017
Haemodynamics Regulate Fibronectin Assembly via PECAM.
Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
What it found
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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.
The trial behind it
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Who cites it
4 citing papers in PubMed, 10 citations in OpenAlex.
- Nanomedicine-based theranostics in atherosclerotic cardiovascular diseases.Journal of biomedical science · 2026Review
- Shear Stress as a Driver of Retinal Müller Glia Survival and Fibrotic Reprogramming.Cell biochemistry and function · 2026Article
- EphA2 signaling within integrin adhesions regulates fibrillar adhesion elongation and fibronectin deposition.Matrix biology : journal of the International Society for Matrix Biology · 2021Article
- Developing a Reliable Mouse Model for Cancer Therapy-Induced Cardiovascular Toxicity in Cancer Patients and Survivors.Frontiers in cardiovascular medicine · 2018Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
Abstract
Fibronectin (FN) assembly and fibrillogenesis are critically important in both development and the adult organism, but their importance in vascular functions is not fully understood. Here we identify a novel pathway by which haemodynamic forces regulate FN assembly and fibrillogenesis during vascular remodelling. Induction of disturbed shear stress in vivo and in vitro resulted in complex FN fibril assembly that was dependent on the mechanosensor PECAM. Loss of PECAM also inhibited the cell-intrinsic ability to remodel FN. Gain- and loss-of-function experiments revealed that PECAM-dependent RhoA activation is required for FN assembly. Furthermore, PECAM
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Registered trials
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