ReviewActa physiologica (Oxford, England)2013
Tonic regulation of vascular permeability.
Review in Acta physiologica (Oxford, England), 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 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
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
38 citing papers in PubMed, 78 citations in OpenAlex.
- Basal insulin peglispro versus insulin glargine in insulin-naïve type 2 diabetes: IMAGINE 2 randomized trial.Diabetes, obesity & metabolism · 2016Trial
- Endothelial Surface Glycocalyx in Vascular Functions and Diseases.Advances in experimental medicine and biology · 2026Review
- Impact of Matrix Gel Variations on Primary Culture of Microvascular Endothelial Cell Function.Microcirculation (New York, N.Y. : 1994) · 2024Article
- Simulation and Modeling of the Adhesion ofPathogens (Basel, Switzerland) · 2024Article
- Review
- Cortactin is in a complex with VE-cadherin and is required for endothelial adherens junction stability through Rap1/Rac1 activation.Scientific reports · 2024Article
- DOCK4 Regulation of Rho GTPases Mediates Pulmonary Vascular Barrier Function.Arteriosclerosis, thrombosis, and vascular biology · 2022Article
- Review
- Permeability of the Endothelial Barrier: Identifying and Reconciling Controversies.Trends in molecular medicine · 2021Review
- Advances in the Starling Principle and Microvascular Fluid Exchange; Consequences and Implications for Fluid Therapy.Frontiers in veterinary science · 2021Review
- Article
- Article
- p90RSK-MAGI1 Module Controls Endothelial Permeability by Post-translational Modifications of MAGI1 and Hippo Pathway.Frontiers in cardiovascular medicine · 2020Article
- Ovulation: Parallels With Inflammatory Processes.Endocrine reviews · 2019Review
- Epac1Acta physiologica (Oxford, England) · 2019Article
- Histamine causes endothelial barrier disruption via CaScientific reports · 2018Article
- Extracellular adenosine-induced Rac1 activation in pulmonary endothelium: Molecular mechanisms and barrier-protective role.Journal of cellular physiology · 2018Article
- Integrin αExperimental physiology · 2018Article
- Insulin regulates multiple signaling pathways leading to monocyte/macrophage chemotaxis into the wound tissue.Biology open · 2018Article
- Endothelial cell-cell adhesion and signaling.Experimental cell research · 2017Review
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Our major theme is that the layered structure of the endothelial barrier requires continuous activation of signalling pathways regulated by sphingosine-1-phosphate (S1P) and intracellular cAMP. These pathways modulate the adherens junction, continuity of tight junction strands, and the balance of synthesis and degradation of glycocalyx components. We evaluate recent evidence that baseline permeability is maintained by constant activity of mechanisms involving the small GTPases Rap1 and Rac1. In the basal state, the barrier is compromised when activities of the small GTPases are reduced by low S1P supply or delivery. With inflammatory stimulus, increased permeability can be understood in part as the action of signalling to reduce Rap1 and Rac1 activation. With the hypothesis that microvessel permeability and selectivity under both normal and inflammatory conditions are regulated by mechanisms that are continuously active, it follows that when S1P or intracellular cAMP are elevated at the time of inflammatory stimulus, they can buffer changes induced by inflammatory agents and maintain normal barrier stability. When endothelium is exposed to inflammatory conditions and subsequently exposed to elevated S1P or intracellular cAMP, the same processes restore the functional barrier by first re-establishing the adherens junction, then modulating tight junctions and glycocalyx. In more extreme inflammatory conditions, loss of the inhibitory actions of Rac1-dependent mechanisms may promote expression of more inflammatory endothelial phenotypes by contributing to the up-regulation of RhoA-dependent contractile mechanisms and the sustained loss of surface glycocalyx allowing access of inflammatory cells to the endothelium.
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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.