ReviewAnnals of intensive care2025
Vascular leakage during circulatory failure: physiopathology, impact and treatments.
Review in Annals of intensive care, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers, 1 of them a synthesis that pooled it.
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.
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Who cites it
10 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Targeting capillary leak in experimental sepsis and endotoxemia: a systematic review of therapeutic agents, methods and models in animal studies.Critical care (London, England) · 2026Pooled it
- Molecular Mechanisms Governing Vascular Function in Heart Failure.Arteriosclerosis, thrombosis, and vascular biology · 2026Review
- DAMPs, PAMPs, and Alarmins: From Mechanism to Therapy.MedComm · 2026Review
- High vasopressor doses are associated with decreased tissue oxygenation in critically ill patients: a secondary analysis of a prospective cohort.Critical care (London, England) · 2026Article
- Comparison of norepinephrine with a combined non-catecholaminergic therapy in a porcine model of refractory cardiac arrest resuscitated with VA-ECMO.Intensive care medicine experimental · 2026Article
- Liquid Metal Microrobots for Magnetically Guided Transvascular Navigation.Advanced materials (Deerfield Beach, Fla.) · 2026Article
- Thrombosis-related gene signature predicts prostate cancer recurrence and immune therapy: insights from retrospective cohorts, bioinformatics, and experimental validation.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026Article
- Immunomodulatory Roles and Clinical Significance of GZMM and DDX24 in Sepsis: A Multiomics Integrative Analysis With Experimental Validation.Human mutation · 2026Article
- Endothelial barrier and sepsis: mechanisms and potential therapeutic strategies.Military Medical Research · 2026Review
- Subcutaneous interstitial pressure measurement during early septic shock: an exploratory study.Scientific reports · 2025Observational
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
18 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Vascular leakage has emerged as a major factor during circulatory failure. Triggered by the inflammatory process following the recognition of both pathogen-associated molecular patterns (PAMPs) and damage-associated molecular patterns (DAMPs), it worsens circulatory failure through the hypovolemia it induces. It may also crucially participate in secondary microcirculation disorders and organ dysfunctions, due to interstitial edema resulting from extravascular fluid accumulation. Accordingly, fluid balance, i.e., the difference between fluid intake and output, is directly related with outcomes during the different types of shock. Moreover, controlling vascular leakage had beneficial effects in various animal models of circulatory failure. However, despite promising preclinical findings, no routine drug is currently available to control vascular leakage in humans. This review depicts the mechanisms involved in the maintenance of a quiescent endothelium and those implicated in the destabilization of its barrier function in various forms of shocks. It further describes available tools to explore vascular leakage and the most advanced treatments under development.
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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.