ArticleBlood2022
S100A8/A9 drives the formation of procoagulant platelets through GPIbα.
Article in Blood, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 63 papers.
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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
63 citing papers in PubMed, 98 citations in OpenAlex.
- Effects of 660 nm & 808 nm photo-biomodulation on S100A8/A9 in symptomatic pulpitis: a randomized controlled trial.Lasers in medical science · 2026Trial
- Procoagulant platelets: linking coagulation and thromboinflammation in cardiovascular disease.Nature reviews. Cardiology · 2026Review
- A 'Tangled Web' in the CNS: unraveling neutrophil extracellular traps in neurological disorders.Molecular neurodegeneration · 2026Review
- Neutrophil-derived S100A8/A9 impairs megakaryocyte maturation in immune thrombocytopenia.Nature communications · 2026Article
- Platelet hyperactivation drives oxidized mitochondrial DNA-induced neutrophil extracellular traps formation in biliary atresia.JHEP reports : innovation in hepatology · 2026Article
- Immune Cell Composition and Protein Biomarkers Correlate With PRP Treatment Outcomes in Knee Osteoarthritis.Orthopaedic journal of sports medicine · 2026Article
- Neutrophil CD14: expanding the deep vein thrombosis framework.Blood advances · 2026Article
- Plasma proteomics identifies S100A8/A9 as a novel biomarker and therapeutic target for fulminant myocarditis.Journal of advanced research · 2026Article
- Platelet effector functions in inflammation.Research and practice in thrombosis and haemostasis · 2026Review
- Thromboinflammation is associated with high thrombotic risk in patients with newly diagnosed myeloproliferative neoplasms.Leukemia · 2026Article
- Inhibition of SPI1 by ADAP Regulates S100A8/A9 Signaling in Macrophages to Control the Development of Colitis.Inflammation · 2026Article
- Inflammation and iron metabolism dysregulation as hallmarks of COVID-19 severity.Frontiers in immunology · 2026Observational
- N-myc and STAT interactor promotes poly(I:C)-induced pulmonary coagulopathy via STAT3-dependent tissue factor.Frontiers in immunology · 2026Article
- The S100A8/A9-NETosis feedback loop in sepsis: potential mechanisms, immune crosstalk, and therapeutic targeting.Frontiers in immunology · 2026Review
- The mechanism of S100A8/A9 heterodimer promoting atherosclerotic thrombosis.Clinical and experimental medicine · 2025Article
- Gentisic acid ameliorates lumbar disc herniation by regulating M1/M2 Polarization via the MAPK14/S100A9/Rac1/2 pathway.Cell biology and toxicology · 2025Article
- Maximizing Efficacy of Cancer Nanovaccines and Immune Cells Landscape in Responders and Non-Responders to Immunotherapy.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Platelet-activating histone/antihistone IgG complexes in anti-PF4-negative thrombosis and thrombocytopenia syndrome.Blood advances · 2025Observational
- Plasma peptidomics: cutting coagulation down to size.Journal of thrombosis and haemostasis : JTH · 2025Article
- Systemic S100A8/A9 in patients with moderate to severe acute ischemic stroke: Exploratory analysis of inflammation and functional outcome.Brain, behavior, & immunity - health · 2025Article
3 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
23 authors at 5 institutions in 3 countries.
Funding
Abstract
S100A8/A9, also known as "calprotectin" or "MRP8/14," is an alarmin primarily secreted by activated myeloid cells with antimicrobial, proinflammatory, and prothrombotic properties. Increased plasma levels of S100A8/A9 in thrombo-inflammatory diseases are associated with thrombotic complications. We assessed the presence of S100A8/A9 in the plasma and lung autopsies from patients with COVID-19 and investigated the molecular mechanism by which S100A8/A9 affects platelet function and thrombosis. S100A8/A9 plasma levels were increased in patients with COVID-19 and sustained high levels during hospitalization correlated with poor outcomes. Heterodimeric S100A8/A9 was mainly detected in neutrophils and deposited on the vessel wall in COVID-19 lung autopsies. Immobilization of S100A8/A9 with collagen accelerated the formation of a fibrin-rich network after perfusion of recalcified blood at venous shear. In vitro, platelets adhered and partially spread on S100A8/A9, leading to the formation of distinct populations of either P-selectin or phosphatidylserine (PS)-positive platelets. By using washed platelets, soluble S100A8/A9 induced PS exposure but failed to induce platelet aggregation, despite GPIIb/IIIa activation and alpha-granule secretion. We identified GPIbα as the receptor for S100A8/A9 on platelets inducing the formation of procoagulant platelets with a supporting role for CD36. The effect of S100A8/A9 on platelets was abolished by recombinant GPIbα ectodomain, platelets from a patient with Bernard-Soulier syndrome with GPIb-IX-V deficiency, and platelets from mice deficient in the extracellular domain of GPIbα. We identified the S100A8/A9-GPIbα axis as a novel targetable prothrombotic pathway inducing procoagulant platelets and fibrin formation, in particular in diseases associated with high levels of S100A8/A9, such as COVID-19.
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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.