ArticleCardiovascular research2023
Neutrophil inhibition improves acute inflammation in a murine model of viral myocarditis.
Article in Cardiovascular research, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers, 1 of them a synthesis that pooled it.
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Who cites it
46 citing papers in PubMed, 1 synthesis or guideline pooled it, 61 citations in OpenAlex.
- Neutrophil Extracellular Traps in Viral Infections.Pathogens (Basel, Switzerland) · 2025Pooled it
- Neutrophil extracellular traps in cardiovascular disease: Mechanisms and therapeutic implications (Review).International journal of molecular medicine · 2026Review
- Antiviral innate immunity in myocarditis: mechanisms and emerging therapeutics.Experimental & molecular medicine · 2026Review
- Neutrophil depletion exacerbatesFood and waterborne parasitology · 2026Article
- Cardiac immunity and heart repair: Mechanism, challenge, and future direction.Chinese medical journal · 2026Review
- Cell death crosstalk in NET-Driven inflammation: mechanisms, disease contexts, and therapeutic perspectives.Biomarker research · 2026Review
- Review
- The clinicopathologic features of fulminant myocarditis.Journal of advanced research · 2026Article
- PAD4+ neutrophils promote hepatic stellate cell activation and accelerate MASH fibrosis progression viaNET-DNA/TAOK1/MAPK pathways.JCI insight · 2026Article
- Peripheral blood cells and immune checkpoint inhibitor-associated myocarditis: a retrospective clinical study with pharmacovigilance and single-cell analysis.Frontiers in immunology · 2026Article
- Integrated pharmacology and experimental validation reveals potential multiple mechanisms of the neutrophil elastase inhibitor sivelestat in attenuating myocarditis.Frontiers in pharmacology · 2026Article
- Neuromodulation and Copper Chelation Reverse Sleep Fragmentation-Aggravated Myocardial Ischemia-Reperfusion Injury by Targeting NET-Induced Endothelial Cuproptosis.Research (Washington, D.C.) · 2026Article
- Inflammatory responses driven by neutrophil extracellular traps in cardiovascular diseases: molecular mechanisms, emerging biomarkers, and therapeutic targets.Frontiers in immunology · 2026Review
- Short-term outcome and prognostic factors in acute fulminant myocarditis with acute kidney injury patients.Frontiers in medicine · 2026Article
- Precision immunomodulation of viral myocarditis: a spatiotemporal intervention paradigm based on smart biomaterials.Frontiers in immunology · 2026Review
- Therapeutic Targeting of Viral Myocarditis with Natural Products and Herbal Medicines: From Immune-Inflammatory Mechanisms to Clinical Translation.Journal of inflammation research · 2026Review
- The cardiovascular-immune axis: crosstalk and therapy in atherosclerosis, myocarditis and vasculitis.Frontiers in immunology · 2026Review
- Relation Between Neutrophil Count and Left Ventricular Ejection Fraction Following Acute Myocarditis in Adolescents: A Preliminary Study.Children (Basel, Switzerland) · 2025Article
- Neutrophil-to-lymphocyte ratio for risk stratification in acute myocarditis across the left ventricular ejection fraction spectrum.European journal of heart failure · 2025Article
- Prognostic nutritional index in risk of mortality following fulminant myocarditis.Scientific reports · 2025Article
Corrections and comments
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Authors and funding
9 authors at 4 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
aimsViral myocarditis (VM) is an inflammatory pathology of the myocardium triggered by a viral infection that may cause sudden death or heart failure (HF), especially in the younger population. Current treatments only stabilize and improve cardiac function without resolving the underlying inflammatory cause. The factors that induce VM to progress to HF are still uncertain, but neutrophils have been increasingly associated with the negative evolution of cardiac pathologies. The present study investigates the contribution of neutrophils to VM disease progression in different ways. METHODS AND
resultsIn a coxsackievirus B3- (CVB3) induced mouse model of VM, neutrophils and neutrophil extracellular traps (NETs) were prominent in the acute phase of VM as revealed by enzyme-linked immunosorbent assay analysis and immunostaining. Anti-Ly6G-mediated neutrophil blockade starting at model induction decreased cardiac necrosis and leucocyte infiltration, preventing monocyte and Ly6CHigh pro-inflammatory macrophage recruitment. Furthermore, genetic peptidylarginine deiminase 4-dependent NET blockade reduced cardiac damage and leucocyte recruitment, significantly decreasing cardiac monocyte and macrophage presence. Depleting neutrophils with anti-Ly6G antibodies at 7 days post-infection, after the acute phase, did not decrease cardiac inflammation.
conclusionCollectively, these results indicate that the repression of neutrophils and the related NET response in the acute phase of VM improves the pathological phenotype by reducing cardiac inflammation.
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