ArticleScience advances2025
Endothelial CLEC5A drives barrier dysfunction and vascular leakage responsible for lung injury in bacterial pneumonia and sepsis.
Article in Science advances, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed.
- Multiple organ dysfunction syndrome: molecular mechanisms and therapeutic strategies.Signal transduction and targeted therapy · 2026Review
- Transcriptomics and network pharmacology reveal that baicalin alleviates acute lung injury induced by H1N1 via targeting STAT1.Archives of microbiology · 2026Article
- Harnessing NIR-II-responsive Rh single-atom nanozymes for photothermal-catalytic immunomodulation and eradication of drug-resistant biofilms in deep tissues.Materials today. Bio · 2026Article
- Targeting the GPX4-FUNDC1 Interaction with Magnesium Lithospermate B Attenuates Sepsis-Associated Lung Injury.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- The single-cell immune atlas of bacterial pneumonia: from inflammatory cell infiltration to treatable cell states.Frontiers in cellular and infection microbiology · 2026Review
- Big data analytics for CLEC5A dynamics based on single cell genomics and proteomics reveal its diverse functions in human diseases.Nanotheranostics · 2026Article
- Immune-endothelial-coagulation crosstalk as a driver of multi-organ dysfunction in severe viral pneumonia.Frontiers in immunology · 2026Review
- Prevalence and Risk Factors Associated with the Recurrence of Infantile Hemangiomas After Discontinuation of Propranolol: A Systematic Review and Meta-Analysis.Journal of clinical medicine · 2025Review
- Interaction between endothelial injury and immune response in septic shock: from basic research to clinical applications.Frontiers in physiology · 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
13 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Endothelial barrier dysfunction and the resulting vascular injury are responsible for multiorgan failure in sepsis. Myeloid C-type lectin domain family 5 member A (CLEC5A) is a pattern recognition receptor involved in host defense against infection. Mice lacking CLEC5A were resistant to cecal ligation and puncture (CLP)-induced polymicrobial sepsis and lipopolysaccharide (LPS)-induced endotoxemia, as observed by decreased mortality. Single-cell RNA sequencing revealed transcriptomic heterogeneity of vascular endothelial cells in CLEC5A-deficient lungs following CLP. Endothelial-specific knockdown of CLEC5A improved survival of CLP-challenged mice, which was completely ineffective with reexpression of endothelial CLEC5A. The survival benefits were attributed to alleviated inflammatory storm and vascular leakage. Furthermore, endothelial CLEC5A deficiency protected mice against
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