ReviewCells2021
Role of Neutrophils in Cardiac Injury and Repair Following Myocardial Infarction.
Review in Cells, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 129 papers, 3 of them syntheses that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
129 citing papers in PubMed, 3 syntheses or guidelines pooled it.
- Identification of key proteins and pathways in myocardial infarction using machine learning approaches.Scientific reports · 2025Pooled it
- Neutrophil-Enriched Biomarkers and Long-Term Prognosis in Acute Coronary Syndrome: a Systematic Review and Meta-analysis.Journal of cardiovascular translational research · 2024Pooled it
- Cardiac repair after myocardial infarction: A two-sided role of inflammation-mediated.Frontiers in cardiovascular medicine · 2022Pooled it
- Spatially Distinct Bone Marrow Sites Are Asymmetrically Impacted by Inflammatory Cardiovascular Disease.JACC. Basic to translational science · 2026Article
- Increased NETosis in Patients With Heart Failure Is Associated With Macrophage Activation Towards a Proinflammatory Phenotype.Journal of cellular and molecular medicine · 2026Article
- Full-field analysis indicates late reperfusion therapy broadens and mechanically smooths the borderzone during post-infarction inflammation.Acta biomaterialia · 2026Article
- Observational
- SiglecF-expressing neutrophils differentiate from mature neutrophils locally in the heart after myocardial infarction.Experimental hematology · 2026Article
- CBC-Derived Inflammatory Indices and Myocardial Injury Severity at Presentation in Acute Myocardial Infarction: Association and Discriminative Performance.Journal of clinical medicine · 2026Article
- Long-term exposure to wildfire smoke particulate matter and incident stroke: a US nationwide study.European heart journal · 2026Article
- Identification of biomarkers associated with mitochondria and macrophage polarization in acute myocardial infarction: a bioinformatics analysis and validation study.Journal of cardiothoracic surgery · 2026Article
- Ex vivo imaging reveals neutrophil behaviors in the adult zebrafish heart.Journal of cell science · 2026Article
- 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
- β2 adrenergic receptors orchestrate neutrophil demargination and recruitment to the ischemic heart following myocardial infarction.Nature communications · 2026Article
- Circulating Markers of Neutrophil Extracellular Traps for Long-Term Prognosis in Patients With Acute Chest Pain.Journal of the American Heart Association · 2026Article
- Cellular and molecular signals of cardiac wound healing after myocardial infarction.American journal of physiology. Heart and circulatory physiology · 2026Review
- Pediatric heart failure in the era of cardio-immunology: inflammatory-immune context phenotypes, diagnosis, and targeted management.Frontiers in immunology · 2026Review
- The immune-cardiovascular metabolic circuitry in myocardial ischemia-reperfusion injury: from metabolic signal release to spatiotemporal reprogramming.Frontiers in immunology · 2026Review
- Adrenergic receptors on immune cells in cardiovascular disease: signaling plasticity, biased agonism, and therapeutic opportunities.Frontiers in physiology · 2026Review
69 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
1 author.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Neutrophils are first-line responders of the innate immune system. Following myocardial infarction (MI), neutrophils are quickly recruited to the ischemic region, where they initiate the inflammatory response, aiming at cleaning up dead cell debris. However, excessive accumulation and/or delayed removal of neutrophils are deleterious. Neutrophils can promote myocardial injury by releasing reactive oxygen species, granular components, and pro-inflammatory mediators. More recent studies have revealed that neutrophils are able to form extracellular traps (NETs) and produce extracellular vesicles (EVs) to aggravate inflammation and cardiac injury. On the contrary, there is growing evidence showing that neutrophils also exert anti-inflammatory, pro-angiogenic, and pro-reparative effects, thus facilitating inflammation resolution and cardiac repair. In this review, we summarize the current knowledge on neutrophils' detrimental roles, highlighting the role of recently recognized NETs and EVs, followed by a discussion of their beneficial effects and molecular mechanisms in post-MI cardiac remodeling. In addition, emerging concepts about neutrophil diversity and their modulation of adaptive immunity are discussed.
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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.