ReviewJournal of inflammation research2025
Advances in Research on the Release of von Willebrand Factor from Endothelial Cells through the Membrane Attack Complex C5b-9 in Sepsis.
Review in Journal of inflammation research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers, 1 of them a synthesis that pooled it.
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Who cites it
11 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Vascular Complications of Long COVID-From Endothelial Dysfunction to Systemic Thrombosis: A Systematic Review.International journal of molecular sciences · 2025Pooled it
- Fulminant Thromboinflammatory Syndrome Following an Influenza-like Illness in an Adolescent: Clinical Insights from a Case Report.International journal of molecular sciences · 2026Article
- Nanoadjuvant-integrated organic biomaterials for immune engineering: Mechanisms, design strategies, and translational applications.Materials today. Bio · 2026Review
- Mitochondrial calcium uniporter as a biomarker in lung adenocarcinoma: regulation of the immune microenvironment, apoptosis, cell cycle and mitophagy.American journal of cancer research · 2026Article
- Retrospective analysis of von willebrand factor and microthrombus formation in septic shock: associations with TTP-like syndrome and sepsis-induced coagulopathy.American journal of clinical and experimental immunology · 2026Article
- Complement in acute kidney injury: a convergent pathogenic pathway in multifactorial renal damage.Frontiers in immunology · 2026Review
- Pathogenic cytokines in thrombotic microangiopathies: molecular insights and therapeutic targets.Molecular medicine (Cambridge, Mass.) · 2025Review
- Cytokine storm and microvascular fate: mechanistic insights into endothelial injury in thrombotic microangiopathies.Annals of medicine and surgery (2012) · 2025Review
- Recent advances in understanding oxidative stress in sepsis: pathogenic roles and antioxidant therapeutic prospects - a narrative review.Frontiers in pharmacology · 2025Review
- Glial-mediated immune modulation in glaucomatous neurodegeneration: mechanisms and therapeutic implications.Frontiers in immunology · 2025Review
- Sepsis-Induced Endothelial Barrier Dysfunction: Mechanisms, Pathology, and Therapeutic Advances.Research (Washington, D.C.) · 2025Review
Corrections and comments
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Authors and funding
10 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Sepsis, a lethal organ dysfunction syndrome driven by aberrant host responses to infection, intertwines excessive inflammatory responses and dysregulated coagulation processes in its pathophysiology. Emerging research reveals the complement terminal membrane attack complex C5b-9 orchestrates ultralarge von Willebrand factor (ULVWF) release from vascular endothelial cells (ECs) through multifaceted mechanisms: C5b-9 compromises EC membrane integrity, activates calcium influx cascades, and provokes NLRP3 inflammasome signaling, triggering massive exocytosis of ULVWF stored within Weibel-Palade bodies (WPBs). When ADAMTS13 activity falters, undegraded ULVWF complexes with platelets to spawn microthrombi, precipitating microvascular occlusion and multiorgan collapse. Strikingly, elevated plasma von Willebrand factor (vWF) antigen levels in sepsis patients correlate robustly with endothelial injury, thrombocytopenia, and mortality-underscoring C5b-9-driven vWF release as a linchpin of septic coagulopathy. Current therapeutic strategies targeting these pathways, including recombinant ADAMTS13 (rhADAMTS13), N-acetylcysteine (NAC), and complement inhibitors like eculizumab, face limitations in clinical translation, necessitating further validation of their efficacy. Additionally, investigating complement regulatory molecules such as CD59 may unlock novel therapeutic avenues. Deciphering the intricate interplay within the C5b-9-vWF axis and advancing precision therapies hold transformative potential for ameliorating sepsis outcomes.
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