ReviewCardiovascular research2019
Platelets in cardiac ischaemia/reperfusion injury: a promising therapeutic target.
Review in Cardiovascular research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 80 papers.
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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.
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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
80 citing papers in PubMed, 132 citations in OpenAlex.
- Assessment of myocardial salvage in patients with STEMI undergoing thrombolysis: ticagrelor versus clopidogrel.BMC cardiovascular disorders · 2022Trial
- Platelet membrane-fusing MSC-derived apoptotic extracellular vesicles enhanced cardiac repair after ischemia/reperfusion injury.Drug delivery and translational research · 2026Article
- VCAM-1-targeting peptide assemblies protect vascular endothelium and prolong cardiac xenograft survival.Science advances · 2026Article
- Reperfusion injury from a haemodynamic standpoint and role of pressure-controlled reperfusion in avoiding reperfusion injury.European heart journal open · 2026Review
- Effects of serotonin transporters on myocardial cell injury during ischemia/reperfusion in rats.The journal of physiological sciences : JPS · 2026Article
- Endothelial MerTK impairment promotes cardiac dysfunction in the condition of high fat diet.Redox biology · 2026Article
- Comparing anti-platelet and anti-thrombin therapies in the ischaemia-reperfusion injured coronary microcirculation of healthy and diabetic mice.Basic research in cardiology · 2026Article
- TRPM7 Deficiency Protects Against Myocardial Ischemia-Reperfusion Injury by Regulating Intracellular ZnCirculation · 2026Article
- Review
- Enhanced Antiplatelet Activity of Nitrated Fatty Acid Extracts fromMolecules (Basel, Switzerland) · 2026Article
- Predictors of Impaired Reperfusion in ST-Elevation Myocardial Infarction Treated with Primary PCI: Preliminary Results from COMA.NET Project.Diagnostics (Basel, Switzerland) · 2026Article
- Iron-dependent ferroptosis in cardiac microvascular endothelial cells: a key link between dysregulated iron homeostasis and microcirculatory injury during myocardial ischemia-reperfusion.Frontiers in cardiovascular medicine · 2026Review
- Ablation of Slc26a6 Mitigates Myocardial Ischemia/Reperfusion Injury.Biomedicines · 2025Article
- Platelets induce endothelial cell mitochondrial dysfunction in myocardial infarction.Science advances · 2025Article
- Stromal-platelet membrane-inspired nanoparticles (SPIN) for targeted heart repair.Bioactive materials · 2025Article
- Platelet-derived biomimetic nanoplatforms: a promising drug delivery strategy for cardiovascular disease.Journal of nanobiotechnology · 2025Review
- Advancements in nanomedicine for modulating ischemic cardiomyopathy therapy.Materials today. Bio · 2025Review
- Platelet Membrane-Camouflaged Biomimetic Drug Delivery Systems for Ischemia-Reperfusion Injury: Targeted Therapeutic Strategies.Physiological research · 2025Review
- Association Between the Hemoglobin, Albumin, Lymphocyte, and Platelet (HALP) Score and Adverse Outcomes in Critically Ill Patients With Acute Myocardial Infarction: A Retrospective Study and Machine Learning Analysis.Reviews in cardiovascular medicine · 2025Article
- Molecular Mechanisms of Microvascular Obstruction and Dysfunction in Percutaneous Coronary Interventions: From Pathophysiology to Therapeutics-A Comprehensive Review.International journal of molecular sciences · 2025Review
20 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
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Acute myocardial infarction (AMI) is the single leading cause of mortality and morbidity worldwide. A key component of AMI therapy is the timely reopening of occluded vessels to prevent further ischaemic damage to the myocardium. However, reperfusion of the ischaemic myocardium can itself trigger reperfusion injury causing up to 50% of the overall infarct size. In recent years, considerable research has been devoted to understanding the pathogenesis of ischaemia/reperfusion (I/R) injury and platelets have emerged as a major contributing factor. This review summarizes the role of platelets in the pathogenesis of I/R injury and highlights the potential of platelet-directed therapeutics to minimize cardiac I/R injury. Activated platelets infiltrate specifically into the ischaemic/reperfused myocardium and contribute to I/R injury by the formation of microthrombi, enhanced platelet-leucocyte aggregation, and the release of potent vasoconstrictor and pro-inflammatory molecules. This review demonstrates the benefits of platelet inhibition beyond their well-described anti-thrombotic effect and highlights the direct cardioprotective role of anti-platelet drugs. In particular, the inhibition of COX, the P2Y12 receptor and the GPIIb/IIIa receptor has demonstrated the potential to attenuate I/R injury. Moreover, targeting of drug candidates or regenerative cells to the activated platelets accumulated within the ischaemic/reperfused myocardium shows remarkable potential to protect the myocardium from I/R injury. Overall, activated platelets play a key role in the pathogenesis of I/R injury. Their direct inhibition as well as their use as epitopes for site-directed therapy is a unique and promising therapeutic approach for the prevention of I/R injury and ultimately the preservation of cardiac function.
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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.