ArticleCirculation2020
Neutrophil-Derived S100A8/A9 Amplify Granulopoiesis After Myocardial Infarction.
Article in Circulation, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 211 papers, 1 of them a synthesis that pooled it.
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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
211 citing papers in PubMed, 1 synthesis or guideline pooled it, 306 citations in OpenAlex.
- Neutrophil-Enriched Biomarkers and Long-Term Prognosis in Acute Coronary Syndrome: a Systematic Review and Meta-analysis.Journal of cardiovascular translational research · 2024Pooled it
- Effect of interleukin-1 blockade with anakinra on leukocyte count in patients with ST-segment elevation acute myocardial infarction.Scientific reports · 2022Trial
- CKD disrupts cardiac energy metabolism and aggravates cardiac inflammation, oxidative stress, and dysfunction post-infarction.Cardiovascular research · 2026Article
- DAMPs, PAMPs, and Alarmins: From Mechanism to Therapy.MedComm · 2026Review
- Integrative transcriptomic analysis and experimental validation identify GPR97 and PROK2 as novel genes upregulated in acute myocardial infarction.Functional & integrative genomics · 2026Article
- Cardiac immunity and heart repair: Mechanism, challenge, and future direction.Chinese medical journal · 2026Review
- Machine Learning-Based Identification of Exosome-Associated Diagnostic Biomarkers in Acute Myocardial Infarction and in Silico Drug Prioritization.Cardiovascular drugs and therapy · 2026Article
- Association between the Neutrophil-to-HDL-Cholesterol Ratio and Myocardial Infarction: A Cross-Sectional Study.Arquivos brasileiros de cardiologia · 2026Article
- Myocardial Immune Niches in Homeostasis and Inflammation.Immunological reviews · 2026Review
- Empagliflozin-pretreated mesenchymal stem cell-derived extracellular vesicles facilitate cardiac repair via AGGF1.Journal of nanobiotechnology · 2026Article
- Neutrophil-derived S100A8/A9 impairs megakaryocyte maturation in immune thrombocytopenia.Nature communications · 2026Article
- Plasma alarmin S100A8/A9 serves as a potential biomarker of major adverse cardiovascular events after acute myocardial infarction.Cardiovascular diagnosis and therapy · 2026Article
- Platelet hyperactivation drives oxidized mitochondrial DNA-induced neutrophil extracellular traps formation in biliary atresia.JHEP reports : innovation in hepatology · 2026Article
- scRNA-seq analysis shows neutrophil extracellular traps as drivers of obstruction-induced intestinal damage in rats.Communications biology · 2026Article
- β2 adrenergic receptors orchestrate neutrophil demargination and recruitment to the ischemic heart following myocardial infarction.Nature communications · 2026Article
- Irgm1 Improves Postinfarction Cardiac Repair by Promoting Neutrophil Clearance and Efferocytosis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- S100A8/A9-amplified inflammation (TNF-α/IL-1β) in the bone marrow of tumor-bearing host disrupts early B cell development.Cell & bioscience · 2026Article
- Plasma proteomics identifies S100A8/A9 as a novel biomarker and therapeutic target for fulminant myocarditis.Journal of advanced research · 2026Article
- The role of inflammation and coronary artery lesion severity in patients undergoing percutaneous coronary intervention: a retrospective cohort study.BMC cardiovascular disorders · 2026Article
- Neutrophil heterogeneity in Kawasaki disease and multisystem inflammatory syndrome in children.Pediatric research · 2026Review
151 more citing papers are in PubMed but not listed here.
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Authors and funding
20 authors at 1 institution in 1 country.
Funding
Abstract
backgroundMyocardial infarction (MI) triggers myelopoiesis, resulting in heightened production of neutrophils. However, the mechanisms that sustain their production and recruitment to the injured heart are unclear.
methodsUsing a mouse model of the permanent ligation of the left anterior descending artery and flow cytometry, we first characterized the temporal and spatial effects of MI on different myeloid cell types. We next performed global transcriptome analysis of different cardiac cell types within the infarct to identify the drivers of the acute inflammatory response and the underlying signaling pathways. Using a combination of genetic and pharmacological strategies, we identified the sequelae of events that led to MI-induced myelopoiesis. Cardiac function was assessed by echocardiography. The association of early indexes of neutrophilia with major adverse cardiovascular events was studied in a cohort of patients with acute MI.
resultsInduction of MI results in rapid recruitment of neutrophils to the infarct, where they release specific alarmins, S100A8 and S100A9. These alarmins bind to the Toll-like receptor 4 and prime the nod-like receptor family pyrin domain-containing 3 inflammasome in naïve neutrophils and promote interleukin-1β secretion. The released interleukin-1β interacts with its receptor (interleukin 1 receptor type 1) on hematopoietic stem and progenitor cells in the bone marrow and stimulates granulopoiesis in a cell-autonomous manner. Genetic or pharmacological strategies aimed at disruption of S100A8/A9 and their downstream signaling cascade suppress MI-induced granulopoiesis and improve cardiac function. Furthermore, in patients with acute coronary syndrome, higher neutrophil count on admission and after revascularization correlates positively with major adverse cardiovascular disease outcomes.
conclusionsOur study provides novel evidence for the primary role of neutrophil-derived alarmins (S100A8/A9) in dictating the nature of the ensuing inflammatory response after myocardial injury. Therapeutic strategies aimed at disruption of S100A8/A9 signaling or their downstream mediators (eg, nod-like receptor family pyrin domain-containing 3 inflammasome, interleukin-1β) in neutrophils suppress granulopoiesis and may improve cardiac function in patients with acute coronary syndrome.
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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.