ArticleNature communications2017
The podoplanin-CLEC-2 axis inhibits inflammation in sepsis.
Article in Nature communications, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 93 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.
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Who cites it
93 citing papers in PubMed, 139 citations in OpenAlex.
- Thromborepair: the tissue repair partner to thromboinflammation.Blood vessels, thrombosis & hemostasis · 2026Review
- Protein-protein interaction disruption as a next-generation antithrombotic strategy.Journal of thrombosis and thrombolysis · 2026Review
- Receptor homodimerization significantly prolongs the lifetime of ligand-induced cross-linking of CLEC-2 but not GPVI.Blood vessels, thrombosis & hemostasis · 2026Article
- Podoplanin Antibody SZ168 Alleviates Sepsis Inflammation and Macrophage Dysregulation via ERK Signaling.Human mutation · 2026Article
- Stratified assessment of platelets in sepsis: from dynamic counts to functional phenotypes.Frontiers in immunology · 2026Review
- Sepsis-induced immunothrombosis: from cellular crosstalk to multiple organ dysfunction.Frontiers in immunology · 2026Review
- Platelet lipidome alterations in septic shock: a matched case-control study.Research and practice in thrombosis and haemostasis · 2026Article
- Comparative pathogenicity of goose parvovirus across different epidemic lineages in ducklings and goslings.Virulence · 2025Article
- Nanoplatforms in sepsis storm: Multimodal synergy for precision immunomodulation and pathogen neutralizations.Pharmaceutical science advances · 2025Review
- Molecular Mechanisms of Sepsis-Associated Acute Kidney Injury.Journal of the American Society of Nephrology : JASN · 2025Review
- Article
- Humanized murine models of platelet function.Current opinion in hematology · 2025Review
- Molecular control of PDPNhi macrophage subset induction by ADAP as a host defense in sepsis.JCI insight · 2025Article
- Podoplanin and microthrombi in lung injury.Blood vessels, thrombosis & hemostasis · 2025Article
- The C3/C3aR pathway exacerbates acetaminophen-induced mouse liver injury via upregulating podoplanin on the macrophage.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025Article
- Genetic association of lipids characteristics and lipid lowering drug target genes with sepsis.PloS one · 2025Article
- Targeting PDPN enhances antitumor T-cell activity by disrupting β-catenin-mediated PD-L1 expression in melanoma.Frontiers in immunology · 2025Article
- The Crucial Roles of Platelets as Immune Mediators in Sepsis.Journal of inflammation research · 2025Review
- Dynamic regulation of neutrophil immunometabolism by platelet-derived metabolites.Frontiers in immunology · 2025Review
- Knockdown of PDPN in astrocytes reduces hippocampal inflammation in T2DM mice.Frontiers in immunology · 2025Article
33 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
Abstract
Platelets play a critical role in vascular inflammation through the podoplanin and collagen/fibrin receptors, C-type-lectin-like-2 (CLEC-2) and glycoprotein VI (GPVI), respectively. Both receptors regulate endothelial permeability and prevent peri-vascular bleeding in inflammation. Here we show that platelet-specific deletion of CLEC-2 but not GPVI leads to enhanced systemic inflammation and accelerated organ injury in two mouse models of sepsis-intra-peritoneal lipopolysaccharide and cecal ligation and puncture. CLEC-2 deficiency is associated with reduced numbers of podoplanin-expressing macrophages despite increased cytokine and chemokine levels in the infected peritoneum. Pharmacological inhibition of the interaction between CLEC-2 and podoplanin regulates immune cell infiltration and the inflammatory reaction during sepsis, suggesting that activation of podoplanin underlies the anti-inflammatory action of platelet CLEC-2. We suggest podoplanin-CLEC-2 as a novel anti-inflammatory axis regulating immune cell recruitment and activation in sepsis.
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What OpenQuestion holds
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.