ReviewInflammation research : official journal of the European Histamine Research Society ... [et al.]2017
Role of the immune system in cardiac tissue damage and repair following myocardial infarction.
Review in Inflammation research : official journal of the European Histamine Research Society ... [et al.], 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers, 1 of them a synthesis that pooled it.
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.
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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
44 citing papers in PubMed, 1 synthesis or guideline pooled it, 75 citations in OpenAlex.
- Stem cell-derived exosomes in the treatment of acute myocardial infarction in preclinical animal models: a meta-analysis of randomized controlled trials.Stem cell research & therapy · 2022Pooled it
- Article
- Role and relevance of exosome-mediated epigenetic regulation in the pathogenesis, diagnosis and treatment of cardiovascular diseases (Review).Molecular medicine reports · 2026Review
- The dual role of ATF3 in myocardial repair through macrophage regulation.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2025Review
- CD38 connects the heart and brain.Translational psychiatry · 2025Review
- Cell Reprogramming, Transdifferentiation, and Dedifferentiation Approaches for Heart Repair.International journal of molecular sciences · 2025Review
- A Mathematical Exploration of the Effects of Ischemia-Reperfusion Injury After a Myocardial Infarction.Bioengineering (Basel, Switzerland) · 2025Article
- Neural progenitor cell-derived exosomes in ischemia/reperfusion injury in cardiomyoblasts.BMC neuroscience · 2025Article
- Regulatory T cells: a promising new therapeutic target in ventricular remodeling after myocardial infarction.Frontiers in immunology · 2025Review
- SOX9: a key transcriptional regulator in organ fibrosis.Frontiers in pharmacology · 2025Review
- Review
- Inflammation-Targeted Nanomedicines Alleviate Oxidative Stress and Reprogram Macrophages Polarization for Myocardial Infarction Treatment.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- Unveiling Immune Infiltration Characterizing Genes in Hypertrophic Cardiomyopathy Through Transcriptomics and Bioinformatics.Journal of inflammation research · 2024Article
- Crosstalk between myocardial autophagy and sterile inflammation in the development of heart failure.Autophagy reports · 2024Review
- Myocardial infarction in rats was alleviated by MSCs derived from the maternal segment of the human umbilical cord.Frontiers in cell and developmental biology · 2024Article
- Causal role of gut microbiota, serum metabolites, immunophenotypes in myocarditis: a mendelian randomization study.Frontiers in genetics · 2024Article
- Single-cell RNA sequencing reveals S100a9Theranostics · 2024Article
- Communications between macrophages and cardiomyocytes.Cell communication and signaling : CCS · 2023Review
- Micronized Acellular Matrix Biomaterial Leverages Eosinophils for Postinfarct Cardiac Repair.JACC. Basic to translational science · 2023Article
- Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
introductionThe immune system plays a crucial role in the initiation, development, and resolution of inflammation following myocardial infarction (MI). The lack of oxygen and nutrients causes the death of cardiomyocytes and leads to the exposure of danger-associated molecular patterns that are recognized by the immune system to initiate inflammation.
resultsAt the initial stage of post-MI inflammation, the immune system further damages cardiac tissue to clear cell debris. The excessive production of reactive oxygen species (ROS) by immune cells and the inability of the anti-oxidant system to neutralize ROS cause oxidative stress that further aggravates inflammation. On the other hand, the cells of both innate and adaptive immune system and their secreted factors are critically instrumental in the very dynamic and complex processes of regulating inflammation and mediating cardiac repair.
conclusionsIt is important to decipher the balance between detrimental and beneficial effects of the immune system in MI. This enables us to identify better therapeutic targets for reducing the infarct size, sustaining the cardiac function, and minimizing the likelihood of heart failure. This review discusses the role of both innate and adaptive immune systems in cardiac tissue damage and repair in experimental models of 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.