ArticleCirculation2015
Platelet Extracellular Regulated Protein Kinase 5 Is a Redox Switch and Triggers Maladaptive Platelet Responses and Myocardial Infarct Expansion.
Article in Circulation, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT05628974 (Normal Donor Blood Draws for Platelet Studies and Biomarker Evaluation), which is not on this map. Cited by 41 papers, 1 of them a synthesis 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.
Normal Donor Blood Draws for Platelet Studies and Biomarker Evaluation (ND-PLT)
Who cites it
41 citing papers in PubMed, 1 synthesis or guideline pooled it, 70 citations in OpenAlex.
- Six Novel Loci Associated with Circulating VEGF Levels Identified by a Meta-analysis of Genome-Wide Association Studies.PLoS genetics · 2016Pooled it
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- Comparing biomechanical platelet activation in the carotid artery by computational and experimental modeling.Blood vessels, thrombosis & hemostasis · 2026Article
- TNIK as a molecular switch regulating platelet function in hemostasis and hyperlipidemia-associated thrombosis.Blood advances · 2026Article
- FcR γ-chain and platelet hyperactivity.Blood advances · 2025Article
- NADPH oxidase 2 inhibitor GSK2795039 exerts antiplatelet and antithrombotic activity.Scientific reports · 2025Article
- Chronic diseases alter the platelet rheostat to promote hyperreactivity and thrombosis.The Journal of clinical investigation · 2025Article
- Endoplasmic Reticulum Stress-Induced triggering Receptor Expressed on Myeloid Cells 2 (TREM2) Downregulation Exacerbates Platelet Activation and Myocardial Infarction in Patients With Coronary Artery Disease.Journal of the American Heart Association · 2025Article
- Oroxylin A reverses SHP-2 oxidative inactivation in GPVI signaling to suppress platelet activation and thrombus formation.Thrombosis journal · 2025Article
- Cellular and enzymatic features of thrombi in humans are vascular bed dependent.Blood vessels, thrombosis & hemostasis · 2025Article
- Platelet pals: How blood cells shape the future of the aorta.Vascular medicine (London, England) · 2025Article
- High‑fat diet‑induced LCN2 exacerbates myocardial ischemia‑reperfusion injury by enhancing platelet activation.Molecular medicine reports · 2024Article
- Soluble glycoprotein VI predicts abdominal aortic aneurysm growth rate and is a novel therapeutic target.Blood · 2024Article
- Long-lived lung megakaryocytes contribute to platelet recovery in thrombocytopenia models.The Journal of clinical investigation · 2024Article
- New insights into the roles of olfactory receptors in cardiovascular disease.Molecular and cellular biochemistry · 2024Review
- Article
- Bone and Extracellular Signal-Related Kinase 5 (ERK5).Biomolecules · 2024Review
- Panax quinquefolius saponins combined with dual antiplatelet therapy enhanced platelet inhibition with alleviated gastric injury via regulating eicosanoids metabolism.BMC complementary medicine and therapies · 2023Article
- Review
- Platelets at the Vessel Wall in Non-Thrombotic Disease.Circulation research · 2023Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
11 authors at 1 institution in 1 country.
Funding
Abstract
backgroundPlatelets have a pathophysiologic role in the ischemic microvascular environment of acute coronary syndromes. In comparison with platelet activation in normal healthy conditions, less attention is given to mechanisms of platelet activation in diseased states. Platelet function and mechanisms of activation in ischemic and reactive oxygen species-rich environments may not be the same as in normal healthy conditions. Extracellular regulated protein kinase 5 (ERK5) is a mitogen-activated protein kinase family member activated in hypoxic, reactive oxygen species-rich environments and in response to receptor-signaling mechanisms. Prior studies suggest a protective effect of ERK5 in endothelial and myocardial cells after ischemia. We present evidence that platelets express ERK5 and that platelet ERK5 has an adverse effect on platelet activation via selective receptor-dependent and receptor-independent reactive oxygen species-mediated mechanisms in ischemic myocardium. METHODS AND
resultsUsing isolated human platelets and a mouse model of myocardial infarction (MI), we found that platelet ERK5 is activated post-MI and that platelet-specific ERK5(-/-) mice have less platelet activation, reduced MI size, and improved post-MI heart function. Furthermore, the expression of downstream ERK5-regulated proteins is reduced in ERK5(-/-) platelets post-MI.
conclusionsERK5 functions as a platelet activator in ischemic conditions, and platelet ERK5 maintains the expression of some platelet proteins after MI, leading to infarct expansion. This demonstrates that platelet function in normal healthy conditions is different from platelet function in chronic ischemic and inflammatory conditions. Platelet ERK5 may be a target for acute therapeutic intervention in the thrombotic and inflammatory post-MI environment.
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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 Socratic graph.