Trial reportJournal of immunology (Baltimore, Md. : 1950)2014
ARF6 inhibition stabilizes the vasculature and enhances survival during endotoxic shock.
Trial report in Journal of immunology (Baltimore, Md. : 1950), 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 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
33 citing papers in PubMed, 48 citations in OpenAlex.
- Rapid activation of ARF6 after RAF inhibition augments BRAFOncogene · 2026Article
- Tissue-specific targeting of the ARF6 signalling axis for type 2 diabetes and obesity: From mechanism to nanodelivery.Clinical and translational medicine · 2026Review
- Endothelial Arf6 sustains capillary electrical signaling and cerebral blood flow through PIPbioRxiv : the preprint server for biology · 2025Article
- Rapid activation of ARF6 after RAF inhibition augments BRAFV600E and promotes therapy resistance.Research square · 2025Article
- Article
- Robo4 inhibits neovascularization in oxygen-induced retinopathy by regulating ARF6 and VEGF.Human cell · 2025Article
- ARF6 as a Novel Activator of HIF-2α in Pulmonary Arterial Hypertension.American journal of respiratory cell and molecular biology · 2025Article
- Tumour-intrinsic endomembrane trafficking by ARF6 shapes an immunosuppressive microenvironment that drives melanomagenesis and response to checkpoint blockade therapy.Nature communications · 2024Article
- Arf6 is required for endocytosis and filamentous actin assembly during angiogenesis in vitro.Microcirculation (New York, N.Y. : 1994) · 2023Article
- ADP-Ribosylation Factor 6 Pathway Acts as a Key Executor of Mesenchymal Tumor Plasticity.International journal of molecular sciences · 2023Review
- ARF6-dependent endocytic trafficking of the Interferon-γ receptor drives adaptive immune resistance in cancer.bioRxiv : the preprint server for biology · 2023Article
- Molecular Analysis of SARS-CoV-2 Spike Protein-Induced Endothelial Cell Permeability and vWF Secretion.International journal of molecular sciences · 2023Article
- Arf6 Regulates Endocytosis and Angiogenesis by Promoting Filamentous Actin Assembly.bioRxiv : the preprint server for biology · 2023Article
- Platelet-derived extracellular vesicles aggravate septic acute kidney injury via delivering ARF6.International journal of biological sciences · 2023Article
- Heterozygosity for ADP-ribosylation factor 6 suppresses the burden and severity of atherosclerosis.PloS one · 2023Article
- Alterations in gene expressions of Caco-2 cell responses to LPS and ploy(I:C) stimulation.PeerJ · 2023Article
- Article
- The effects of sepsis on endothelium and clinical implications.Cardiovascular research · 2021Article
- Cytohesin-2/ARNO: A Novel Bridge Between Cell Migration and Immunoregulation in Synovial Fibroblasts.Frontiers in immunology · 2021Article
- Preserving Vascular Integrity Protects Mice against Multidrug-Resistant Gram-Negative Bacterial Infection.Antimicrobial agents and chemotherapy · 2020Article
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 3 institutions in 2 countries.
Funding
Abstract
The vascular endothelium responds to infection by destabilizing endothelial cell-cell junctions to allow fluid and cells to pass into peripheral tissues, facilitating clearance of infection and tissue repair. During sepsis, endotoxin and other proinflammatory molecules induce excessive vascular leak, which can cause organ dysfunction, shock, and death. Current therapies for sepsis are limited to antibiotics and supportive care, which are often insufficient to reduce morbidity and prevent mortality. Previous attempts at blocking inflammatory cytokine responses in humans proved ineffective at reducing the pathologies associated with sepsis, highlighting the need for a new therapeutic strategy. The small GTPase ARF6 is activated by a MyD88-ARNO interaction to induce vascular leak through disruption of endothelial adherens junctions. In this study, we show that the MyD88-ARNO-ARF6-signaling axis is responsible for LPS-induced endothelial permeability and is a destabilizing convergence point used by multiple inflammatory cues. We also show that blocking ARF6 with a peptide construct of its N terminus is sufficient to reduce vascular leak and enhance survival during endotoxic shock, without inhibiting the host cytokine response. Our data highlight the therapeutic potential of blocking ARF6 and reducing vascular leak for the treatment of inflammatory conditions, such as endotoxemia.
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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.