ReviewBiomedical reports2025
NETosis in myocardial ischemia-reperfusion injury: From mechanisms to therapies (Review).
Review in Biomedical reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
12 citing papers in PubMed.
- Reduced ALDH2 Activity and Cardiovascular Carbonyl Stress: From Reactive Aldehyde Networks to Coronary Microvascular Obstruction.Cardiovascular toxicology · 2026Review
- Complement Activation by Post-Translationally Modified Proteins: Links to Chronic Inflammation and Autoimmunity.Immunological reviews · 2026Review
- Puerarin alleviates myocardial ischemia-reperfusion injury by enhancing FUNDC1-mediated mitophagy.Molecular and cellular biochemistry · 2026Article
- Article
- Neutrophil Extracellular Traps and Complement Pathways: The Missing Links in Acute Rheumatic Fever and Rheumatic Heart Disease Pathogenesis.Journal of cardiovascular translational research · 2026Review
- Research Trends in Neutrophil Extracellular Traps and Ischemia-Reperfusion Injury: A Dual-Database Bibliometric Analysis from 2013 to 2025.Journal of inflammation research · 2026Article
- Neutrophil-mediated myocardial ischemia-reperfusion injury: mechanisms and potential therapeutic targets.Frontiers in immunology · 2026Review
- Monocytes and neutrophils promote cardiac fibroblast pro-fibrotic phenotypes through IL-6 and MIF.Frontiers in cell and developmental biology · 2026Article
- Inflammatory Mechanisms in Acute Coronary Syndromes: From Pathophysiology to Therapeutic Targets.Cells · 2025Review
- Mixed lineage kinase 3 contributes to myocardial ischemia/reperfusion injury by regulating neutrophil activation.Basic research in cardiology · 2025Article
- It's a Trap!-Potential of Cathepsins in NET Formation.International journal of molecular sciences · 2025Review
- Network Pharmacology Approaches to Myocardial Infarction Reperfusion Injury: Exploring Mechanisms, Pathophysiology, and Novel Therapies.Biomedicines · 2025Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The present review describes the mechanisms of NETosis and its role in myocardial ischemia-reperfusion injury (MIRI), focusing on the release of neutrophil extracellular traps (NETs) by activated neutrophils. NETs, composed of depolymerized chromatin and granule proteins, are crucial for pathogen entrapment, infection control and immune regulation. However, NET formation, linked to neutrophil death (NETosis), exacerbates MIRI by promoting inflammation and tissue damage. To address therapeutic strategies for NETosis in MIRI, several potential clinically significant approaches were explored, including peptidylarginine deaminase 4 inhibition, DNase therapy, antioxidants, inflammation modulation, and antithrombotic treatments, which not only provide novel diagnostic biomarkers and therapeutic targets in MIRI, but are also expected to improve patient prognosis and advance the development of personalised medicine.
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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.