ArticleJournal of molecular and cellular cardiology2024
Neutrophils are indispensable for adverse cardiac remodeling in heart failure.
Article in Journal of molecular and cellular cardiology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.
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Who cites it
42 citing papers in PubMed, 36 citations in OpenAlex.
- Increased NETosis in Patients With Heart Failure Is Associated With Macrophage Activation Towards a Proinflammatory Phenotype.Journal of cellular and molecular medicine · 2026Article
- Carnosinylation of Cardiac Antigens Attenuates Immunogenic Responses and Improves Function in Failing Hearts.Journal of the American Heart Association · 2026Article
- Evaluation of neutrophil oxidative burst capacity in relation to major adverse cardiac events and infection in patients with cardiovascular disease.Clinical research in cardiology : official journal of the German Cardiac Society · 2026Article
- Immunometabolic Remodeling in Ischemic and Non-Ischemic Heart Failure.Journal of cardiovascular translational research · 2026Review
- Molecular imaging of immune and fibrosis targets to guide therapy for repair after myocardial infarction.Nature reviews. Cardiology · 2026Review
- Association between the systemic inflammatory response index and 1-year all-cause mortality in intensive care unit patients with heart failure: a retrospective cohort study.Journal of thoracic disease · 2026Article
- Review
- Clinical significance and prognostic value of high-density lipoprotein cholesterol-based markers in very young patients with coronary artery disease: a retrospective study.Lipids in health and disease · 2026Article
- Identification and verification of biomarkers associated with integrated stress response in heart failure.Scientific reports · 2026Article
- Shared molecular signatures between atrial fibrillation and chronic obstructive pulmonary disease: an integrated bioinformatic analysis with experimental validation.BMC medical genomics · 2026Article
- CXCL10 Regulates Pressure Overload-Induced Heart Failure.JACC. Basic to translational science · 2026Article
- Genetic and epidemiological insights into the role of neutrophil percentage in heart failure risk: a Mendelian randomization and NHANES study.Molecular and cellular biochemistry · 2026Article
- Neutrophil Extracellular Traps in Heart Failure: From Pathophysiological Mechanisms to Therapeutic Targets.Journal of inflammation research · 2026Review
- Association between neutrophil percentage-to-albumin ratio and adverse clinical outcomes after successful percutaneous coronary intervention for chronic total occlusion: a cohort study.Frontiers in immunology · 2026Article
- Inflammatory responses driven by neutrophil extracellular traps in cardiovascular diseases: molecular mechanisms, emerging biomarkers, and therapeutic targets.Frontiers in immunology · 2026Review
- Immune Cell-Mediated Inflammation in Heart Failure: Subset Heterogeneity and Targeted Therapy.International journal of general medicine · 2026Review
- Association Between Systemic Inflammation Response Index, Worsening of Left Ventricular Systolic Function and Prognosis in Patients with Coronary Artery Disease.Journal of inflammation research · 2026Article
- Neutrophil Heterogeneity after Myocardial Infarction.Journal of innate immunity · 2026Review
- Neutrophil-to-Lymphocyte Ratio and Fibroblast Growth Factor 21: Their Role in Early Cardiovascular Involvement in Rheumatoid Arthritis.Journal of clinical medicine · 2025Article
- HearteXplain: explainable prediction of acute heart failure and identification of hematologic biomarkers using EBMs and Morris sensitivity analysis.Scientific reports · 2025Article
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 2 countries.
Funding
Abstract
Persistent immune activation contributes significantly to left ventricular (LV) dysfunction and adverse remodeling in heart failure (HF). In contrast to their well-known essential role in acute myocardial infarction (MI) as first responders that clear dead cells and facilitate subsequent reparative macrophage polarization, the role of neutrophils in the pathobiology of chronic ischemic HF is poorly defined. To determine the importance of neutrophils in the progression of ischemic cardiomyopathy, we measured their production, levels, and activation in a mouse model of chronic HF 8 weeks after permanent coronary artery ligation and large MI. In HF mice, neutrophils were more abundant both locally in failing myocardium (more in the border zone) and systemically in the blood, spleen, and bone marrow, together with increased BM granulopoiesis. There were heightened stimuli for neutrophil recruitment and trafficking in HF, with increased myocardial expression of the neutrophil chemoattract chemokines CXCL1 and CXCL5, and increased neutrophil chemotactic factors in the circulation. HF neutrophil NETotic activity was increased in vitro with coordinate increases in circulating neutrophil extracellular traps (NETs) in vivo. Neutrophil depletion with either antibody-based or genetic approaches abrogated the progression of LV remodeling and fibrosis at both intermediate and late stages of HF. Moreover, analogous to murine HF, the plasma milieu in human acute decompensated HF strongly promoted neutrophil trafficking. Collectively, these results support a key tissue-injurious role for neutrophils and their associated cytotoxic products in ischemic cardiomyopathy and suggest that neutrophils are potential targets for therapeutic immunomodulation in this disease.
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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.