ArticleAmerican journal of respiratory cell and molecular biology2021
A Translational Investigation of IFN-α and STAT1 Signaling in Endothelial Cells during Septic Shock Provides Therapeutic Perspectives.
Article in American journal of respiratory cell and molecular biology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 12 citations in OpenAlex.
- Endothelial JAML inhibits inflammation and atherosclerosis through TRIM25-mediated STAT1 ubiquitination.Cellular & molecular biology letters · 2026Article
- ATG5 negatively regulates grass carp reovirus-induced immune-inflammatory response by degrading RIG-I and MDA5.Journal of virology · 2025Article
- Interferons prime the endothelium for toll-like receptor-mediated thrombin generation.Journal of thrombosis and haemostasis : JTH · 2024Article
- A model of porcine polymicrobial septic shock.Intensive care medicine experimental · 2023Article
- How to manage coagulopathies in critically ill patients.Intensive care medicine · 2023Review
- Review
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- The Endothelium Is in Shock and IFN-α/STAT1 Signaling Is to Blame.American journal of respiratory cell and molecular biology · 2021Article
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Authors and funding
13 authors at 5 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Septic shock and disseminated intravascular coagulation (DIC) are known to be characterized by an endothelial cell dysfunction. The molecular mechanisms underlying this relationship are, however, poorly understood. In this work, we aimed to investigate human circulating IFN-α in patients with septic shock-induced DIC and tested the potential role of endothelial Stat1 (signal transducer and activator of transcription 1) as a therapeutic target in a mouse model of sepsis. For this, circulating type I, type II, and type III IFNs and procoagulant microvesicles were quantified in a prospective cohort of patients with septic shock. Next, we used a septic shock model induced by cecal ligation and puncture in wild-type mice, in Ifnar1 (type I IFN receptor subunit 1)-knockout mice, and in Stat1 conditional knockout mice. In human samples, we observed higher concentrations of circulating IFN-α and IFN-α1 in patients with DIC compared with patients without DIC, whereas concentrations of IFN-β, IFN-γ, IFN-λ1, IFN-λ2, and IFN-λ3 were not different. IFN-α concentration was positively correlated with CD105 microvesicle concentrations, reflecting endothelial injury. In Ifnar1
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