ReviewFrontiers in immunology2025
Immune in myocardial ischemia/reperfusion injury: potential mechanisms and therapeutic strategies.
Review in Frontiers in immunology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed.
- Dexmedetomidine Attenuates Myocardial Ischemia/Reperfusion Injury by Inhibiting DNMT3B-Mediated Hypermethylation of the KLF4 Promoter.Cardiovascular drugs and therapy · 2026Article
- Potential Relationship Between YTHDF3 and CFTR in Myocardial Ischemia-Reperfusion Injury.Journal of cellular and molecular medicine · 2026Article
- Shenqi Granules Enhance Recovery from Myocardial Ischemia-Reperfusion Injury by Downregulating MMP9 and ADH1C.Pharmaceuticals (Basel, Switzerland) · 2026Article
- Neutrophil-mediated myocardial ischemia-reperfusion injury: mechanisms and potential therapeutic targets.Frontiers in immunology · 2026Review
- FN1 governs global protein lactylation in acute myocardial infarction: a metabolic-epigenetic axis driving cardiac injury and impeding stem cell repair.Frontiers in cell and developmental biology · 2026Article
- Immune Mechanisms in Myocardial Remodeling Following Myocardial Infarction: Focusing on Regulatory Networks of T Cell Responses.Journal of inflammation research · 2026Review
- Mitochondrial Permeability Transition Pore: The Cardiovascular Disease's Molecular Achilles Heel.Biomedicines · 2025Review
- Mixed lineage kinase 3 contributes to myocardial ischemia/reperfusion injury by regulating neutrophil activation.Basic research in cardiology · 2025Article
- Network Pharmacology Approaches to Myocardial Infarction Reperfusion Injury: Exploring Mechanisms, Pathophysiology, and Novel Therapies.Biomedicines · 2025Review
Corrections and comments
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Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Myocardial infarction (MI), which is characterized by high morbidity and mortality, is a serious threat to human life and health, and timely reperfusion therapy to save ischemic myocardium is currently the most effective intervention. Although reperfusion therapy effectively restores coronary blood flow and maximally limits the infarct size, it triggers additional cell death and tissue damage, which is known as myocardial ischemia/reperfusion injury (MIRI). Multiple immune cells are present in the reperfusion area, executing specific functions and engaging in crosstalk during diverse stages, constituting a complex immune microenvironment involved in tissue repair and regeneration after MIRI. Immunotherapy brings new hope for treating ischemic heart disease by modulating the immune microenvironment. In this paper, we explore the regulatory roles of various immune cells during MIRI and the close relationship between different cell deaths and the immune microenvironment. In addition, we present the current status of research on targeting the immune system to intervene in MIRI, with the expectation of providing a basis for achieving clinical translation.
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