ReviewFrontiers in immunology2025
The endothelial-immunothrombotic storm in viral sepsis: lessons from COVID-19.
Review in Frontiers in immunology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 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
6 citing papers in PubMed.
- The Diabetes-Viral Respiratory Syndemic: Pathophysiological Insights and Precision Management: A Scoping Review.Medicina (Kaunas, Lithuania) · 2026Article
- Article
- Serum Calprotectin in Hospitalized Patients with COVID-19 in Relation to High-Dimensional Serum Proteomic Patterns.International journal of molecular sciences · 2026Observational
- Admission D-Dimer for Early Risk Stratification of in-Hospital Mortality in Adults with Non-HIV Cryptococcal Meningitis: A Retrospective Cohort Study.Infection and drug resistance · 2026Article
- Immune-endothelial-coagulation crosstalk as a driver of multi-organ dysfunction in severe viral pneumonia.Frontiers in immunology · 2026Review
- mFrontiers in immunology · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Taking COVID-19 as an illustrative example, this review systematically elucidates the central pathological mechanism of viral sepsis, termed the endothelial-immunothrombotic storm. This mechanism is initiated by the direct viral infection of endothelial cells, which provokes excessive immune activation and disrupts coagulation through immunothrombosis, including cytokine storms, NETosis, and complement activation. Meanwhile, these processes establish a vicious cycle leading to multiple organ failure. Compared with classical bacterial sepsis, viral sepsis exhibits distinctive features such as interferon dysregulation, direct endothelial damage, a hypercoagulable state, and T-cell exhaustion. This review integrates the latest research findings, contrasts the pathophysiological differences between viral and bacterial sepsis, and proposes precision strategies focused on endothelial protection, immune modulation, and anticoagulation. Finally, we discuss the clinical translational prospects of these approaches and suggests directions for future research.
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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 Socratic graph.