ReviewBirth defects research. Part C, Embryo today : reviews2016
Membrane-mediated regulation of vascular identity.
Review in Birth defects research. Part C, Embryo today : reviews, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
10 citing papers in PubMed, 19 citations in OpenAlex.
- Changes in vascular identity during vascular remodeling.JVS-vascular science · 2025Article
- A surgeon-scientist's approach to improving arteriovenous fistula patency.JVS-vascular science · 2024Article
- Temporospatial inhibition of Erk signaling is required for lymphatic valve formation.Signal transduction and targeted therapy · 2023Article
- Environmental and intrinsic modulations of venous differentiation.Cellular and molecular life sciences : CMLS · 2022Article
- Review
- EphB4 signaling maintains the contractile phenotype of adult venous smooth muscle cells.American journal of translational research · 2020Article
- Stimulation of Caveolin-1 Signaling Improves Arteriovenous Fistula Patency.Arteriosclerosis, thrombosis, and vascular biology · 2019Article
- Molecular identity of arteries, veins, and lymphatics.Journal of vascular surgery · 2019Review
- Pathogenic variant in EPHB4 results in central conducting lymphatic anomaly.Human molecular genetics · 2018Article
- Improving the Outcome of Vein Grafts: Should Vascular Surgeons Turn Veins into Arteries?Annals of vascular diseases · 2017Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 4 institutions in 4 countries.
Funding
Abstract
Vascular diseases span diverse pathology, but frequently arise from aberrant signaling attributed to specific membrane-associated molecules, particularly the Eph-ephrin family. Originally recognized as markers of embryonic vessel identity, Eph receptors and their membrane-associated ligands, ephrins, are now known to have a range of vital functions in vascular physiology. Interactions of Ephs with ephrins at cell-to-cell interfaces promote a variety of cellular responses such as repulsion, adhesion, attraction, and migration, and frequently occur during organ development, including vessel formation. Elaborate coordination of Eph- and ephrin-related signaling among different cell populations is required for proper formation of the embryonic vessel network. There is growing evidence supporting the idea that Eph and ephrin proteins also have postnatal interactions with a number of other membrane-associated signal transduction pathways, coordinating translation of environmental signals into cells. This article provides an overview of membrane-bound signaling mechanisms that define vascular identity in both the embryo and the adult, focusing on Eph- and ephrin-related signaling. We also discuss the role and clinical significance of this signaling system in normal organ development, neoplasms, and vascular pathologies.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.