ReviewJournal of the American Heart Association2023
Impact of Reperfusion on Temporal Immune Cell Dynamics After Myocardial Infarction.
Review in Journal of the American Heart Association, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 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
37 citing papers in PubMed, 37 citations in OpenAlex.
- Full-field analysis indicates late reperfusion therapy broadens and mechanically smooths the borderzone during post-infarction inflammation.Acta biomaterialia · 2026Article
- Benign vs. malignant pulmonary nodules: pleural adhesion risks and predictors.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2026Article
- Macrophages and the Survival of Cardiomyocytes After Myocardial Infarction.Arteriosclerosis, thrombosis, and vascular biology · 2026Review
- Dynamic changes in OTULIN and progranulin levels in experimental myocardial infarction and cardiac remodeling.Histochemistry and cell biology · 2026Article
- FTO-mediated m6A demethylation of TRIM21 regulates macrophage polarization and attenuates myocardial ischemia-reperfusion injury.Immunologic research · 2026Article
- KLF2 Promotes Neutrophil Apoptosis in Mice with Myocardial ischemia-reperfusion Injury by Upregulating Notch1.Cell biochemistry and biophysics · 2026Article
- Ferulic acid in combination with ginsenoside Rb1 alleviates myocardial no-reflow by inhibiting platelet HMGB1 release and NET formation.Chinese medicine · 2026Article
- The immune-cardiovascular metabolic circuitry in myocardial ischemia-reperfusion injury: from metabolic signal release to spatiotemporal reprogramming.Frontiers in immunology · 2026Review
- The role of the bidirectional regulatory network between immune cells and stromal cells in cardiac repair and fibrosis following myocardial infarction.Frontiers in immunology · 2026Review
- Sensing succinate: SUCNR1 as a context-dependent metabolic and cellular signal integrator.Frontiers in molecular biosciences · 2026Review
- Multifaceted mechanisms of unconventional T cells in ischemia-reperfusion injury.Frontiers in immunology · 2026Review
- Myocardial ischemia-reperfusion injury after acute myocardial infarction: spatiotemporal mechanisms and endotype-matched multi-target modulation by compounds from traditional Chinese medicine.Frontiers in cardiovascular medicine · 2026Review
- Myocardial Infarction in Murine Models of Obesity and Related Metabolic Disorders: The Role of Inflammation.International journal of molecular sciences · 2025Review
- CTLA-4-Ig therapy preserves cardiac function following myocardial infarction with reperfusion.Cardiovascular research · 2025Article
- S100A8/9-NLRP3-mediated chronic unresolved inflammation drives cardiac pathologies following invasive pneumococcal disease.Experimental & molecular medicine · 2025Article
- Review
- Empagliflozin restores cardiac metabolism and suppresses immune activation in acute myocardial infarction.Atherosclerosis · 2025Article
- Specialized Pro-Resolving Mediators as Emerging Players in Cardioprotection: From Inflammation Resolution to Therapeutic Potential.Acta physiologica (Oxford, England) · 2025Review
- Engineered neutrophil membrane-camouflaged nanocomplexes for targeted siRNA delivery against myocardial ischemia reperfusion injury.Journal of nanobiotechnology · 2025Article
- Evidence and perspectives on miRNA, circRNA, and lncRNA in myocardial ischemia-reperfusion injury: a bibliometric study.Journal of cardiothoracic surgery · 2025Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Excessive inflammation and impaired healing of cardiac tissue following a myocardial infarction (MI) can drive the development of heart failure. Cardiac repair begins immediately after the onset of MI and continues for months. The repair process can be divided into the following 3 overlapping phases, each having distinct functions and sequelae: the inflammatory phase, the proliferative phase, and the maturation phase. Macrophages, neutrophils, and lymphocytes are present in the myocardium throughout the repair process and govern the duration and function of each of these phases. However, changes in the functions of these cell types across each phase are poorly characterized. Numerous immunomodulatory therapies that specifically target inflammation have been developed for promoting cardiac repair and preventing heart failure after MI. However, these treatments have been largely unsuccessful in large-scale clinical randomized controlled trials. A potential explanation for this failure is the lack of a thorough understanding of the time-dependent evolution of the functions of immune cells after a major cardiovascular event. Failure to account for this temporal plasticity in cell function may reduce the efficacy of immunomodulatory approaches that target cardiac repair. This review is concerned with how the functions of different immune cells change with time following an MI. Improved understanding of the temporal changes in immune cell function is important for the future development of effective and targeted treatments for preventing heart failure after MI.
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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.