ArticleJCI insight2020
Monocyte upregulation of podoplanin during early sepsis induces complement inhibitor release to protect liver function.
Article in JCI insight, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 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
18 citing papers in PubMed, 28 citations in OpenAlex.
- Stratified assessment of platelets in sepsis: from dynamic counts to functional phenotypes.Frontiers in immunology · 2026Review
- Transducin-like enhancer of split 3 protects against lipopolysaccharide-induced inflammation through DEAD-box helicase 5-activating transcription factor 1-protein phosphatase 2 regulatory subunit 5A signaling.Journal of advanced research · 2026Article
- Neutrophil membrane-coated nanoparticles for targeted therapy.Discover nano · 2025Review
- Sepsis and the Liver.Diseases (Basel, Switzerland) · 2025Review
- 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
- C-type lectin-like receptor 2: roles and drug target.Thrombosis journal · 2024Review
- Platelet ITGA2B inhibits caspase-8 and Rip3/Mlkl-dependent platelet death though PTPN6 during sepsis.iScience · 2023Article
- Podoplanin and CLEC-2 levels in patients with COVID-19.Research and practice in thrombosis and haemostasis · 2023Article
- CSF-1 and Notch signaling cooperate in macrophage instruction and tissue repair during peripheral limb ischemia.Frontiers in immunology · 2023Article
- Platelet transfusions in a murine model of neonatal polymicrobial sepsis: Divergent effects on inflammation and mortality.Transfusion · 2022Article
- Neutrophil membrane-mimicking nanodecoys with intrinsic anti-inflammatory properties alleviate sepsis-induced acute liver injury and lethality in a mouse endotoxemia model.Materials today. Bio · 2022Article
- Curcumin-Based Inhibitors of Thrombosis and Cancer Metastasis Promoting Factor CLEC 2 from Traditional Medicinal SpeciesEvidence-based complementary and alternative medicine : eCAM · 2022Article
- The Role of Podoplanin in the Immune System and Inflammation.Journal of inflammation research · 2022Review
- Serum C1q Levels Have Prognostic Value for Sepsis and are Related to the Severity of Sepsis and Organ Damage.Journal of inflammation research · 2021Article
- CLEC-2 Prevents Accumulation and Retention of Inflammatory Macrophages During Murine Peritonitis.Frontiers in immunology · 2021Article
- CLEC-2-dependent platelet subendothelial accumulation by flow disturbance contributes to atherogenesis in mice.Theranostics · 2021Article
- Podoplanin Drives Motility of Active MacrophageFrontiers in immunology · 2021Article
- Elevated Soluble Podoplanin Associates with Hypercoagulability in Patients with Nephrotic Syndrome.Clinical and applied thrombosis/hemostasis : official journal of the International Academy of Clinical and Applied Thrombosis/HemostasisArticle
Corrections and comments
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Authors and funding
12 authors at 2 institutions in 2 countries.
Funding
Abstract
Multiple organ failure in sepsis is a progressive failure of several interdependent organ systems. Liver dysfunction occurs early during sepsis and is directly associated with patient death; however, the underlying mechanism of liver dysfunction is unclear. Platelet transfusion benefits patients with sepsis, and inhibition of complement activation protects liver function in septic animals. Herein, we explored the potential link between platelets, complement activation, and liver dysfunction in sepsis. We found that deletion of platelet C-type lectin-like receptor 2 (CLEC-2) exacerbated liver dysfunction in early sepsis. Platelet CLEC-2-deficient mice exhibited higher complement activation, more severe complement attack in the liver, and lower plasma levels of complement inhibitors at early time points after E. coli infection. Circulating monocytes expressed the CLEC-2 ligand podoplanin in early sepsis, and podoplanin binding induced release of complement inhibitors from platelets. Injection of complement inhibitors released from platelets reduced complement attack and attenuated liver dysfunction in septic mice. These findings indicate a new function of platelets in the regulation of complement activation during 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.