ArticleArteriosclerosis, thrombosis, and vascular biology2022
Neutrophil-Derived Protein S100A8/A9 Alters the Platelet Proteome in Acute Myocardial Infarction and Is Associated With Changes in Platelet Reactivity.
Article in Arteriosclerosis, thrombosis, and vascular biology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 33 papers, 1 of them a synthesis that pooled it.
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
33 citing papers in PubMed, 1 synthesis or guideline pooled it, 57 citations in OpenAlex.
- Toward standardization and a concerted vision for platelet proteomics research: communication from the SSC of the ISTH.Journal of thrombosis and haemostasis : JTH · 2025Guideline
- Platelets and inflammation-insights from platelet non-coding RNA content and release in the Bruneck study and the PACMAN-AMI trial.Cardiovascular research · 2025Trial
- Circulating S100A8/A9 drives faster platelet COX-1 recovery via MRP4, impairing the duration of aspirin response.Blood advances · 2026Article
- Thromboinflammation is associated with high thrombotic risk in patients with newly diagnosed myeloproliferative neoplasms.Leukemia · 2026Article
- The S100A8/A9-NETosis feedback loop in sepsis: potential mechanisms, immune crosstalk, and therapeutic targeting.Frontiers in immunology · 2026Review
- Identification of neutrophil extracellular traps-related genes for the diagnosis of acute myocardial infarction based on bioinformatics and experimental verification.Journal of inflammation (London, England) · 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
- Low-Molecular-Weight Fucoidan Inhibits Thromboinflammation and Ameliorates Deep Vein Thrombosis via Targeting S100A8/A9.Marine drugs · 2025Article
- Extracellular vesicle-bound S100A8/A9 is differentially expressed in septic shock and prompts acute lung injury.Respiratory research · 2025Article
- Disseminated intravascular coagulation: cause, molecular mechanism, diagnosis, and therapy.MedComm · 2025Review
- A review of natural compounds to regulate platelet aggregation: molecular mechanism and research advance.Frontiers in pharmacology · 2025Review
- Neutrophil extracellular traps: a catalyst for atherosclerosis.Molecular and cellular biochemistry · 2024Review
- Novel Long Noncoding RNACirculation · 2024Article
- S100A9 deletion in microglia/macrophages ameliorates brain injury through the STAT6/PPARγ pathway in ischemic stroke.CNS neuroscience & therapeutics · 2024Article
- Advances in the study of S100A9 in cardiovascular diseases.Cell proliferation · 2024Review
- Preliminary clinical analysis and pathway study of S100A8 as a biomarker for the diagnosis of acute deep vein thrombosis.Scientific reports · 2024Article
- Computational Deciphering of the Role of S100A8 and S100A9 Proteins and Their Changes in the Structure Assembly Influences Their Interaction with TLR4, RAGE, and CD36.The protein journal · 2024Article
- The 2023 Report on the Proteome from the HUPO Human Proteome Project.Journal of proteome research · 2024Review
- How can we use proteomics to learn more about platelets?Platelets · 2023Article
- A positive feedback cycle between the alarmin S100A8/A9 and NLRP3 inflammasome-GSDMD signalling reinforces the innate immune response in Candida albicans keratitis.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2023Article
Corrections and comments
- Commented on by
- Erratum issued
Authors and funding
17 authors at 5 institutions in 3 countries.
Funding
Abstract
objectivePlatelets are central to acute myocardial infarction (MI). How the platelet proteome is altered during MI is unknown. We sought to describe changes in the platelet proteome during MI and identify corresponding functional consequences. Approach and Results: Platelets from patients experiencing ST-segment-elevation MI (STEMI) before and 3 days after treatment (n=30) and matched patients with severe stable coronary artery disease before and 3 days after coronary artery bypass grafting (n=25) underwent quantitative proteomic analysis. Elevations in the proteins S100A8 and S100A9 were detected at the time of STEMI compared with stable coronary artery disease (S100A8: FC, 2.00; false discovery rate, 0.05; S100A9: FC, 2.28; false discovery rate, 0.005). During STEMI, only S100A8 mRNA and protein levels were correlated in platelets (
conclusionsLeukocyte-to-platelet protein transfer may occur in a thromboinflammatory environment such as STEMI. Plasma S100A8/A9 was negatively associated with platelet reactivity. These findings highlight neutrophils as potential modifiers for thrombotic therapies in coronary artery disease.
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Registered trials
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