ReviewMediators of inflammation2013
Danger signals in the initiation of the inflammatory response after myocardial infarction.
Review in Mediators of inflammation, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 78 papers.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
78 citing papers in PubMed, 122 citations in OpenAlex.
- Cardiomyocyte-specific depletion of integrin α3 preserves cardiac function after myocardial infarction.Basic research in cardiology · 2026Article
- Beyond Reperfusion: Early Molecular Drivers and Therapeutic Opportunities in Acute Post-Infarction Cardiac Fibrosis.International journal of molecular sciences · 2026Review
- The Role of Neutrophil, Monocyte and Macrophage Calprotectin and S100A12 in the Fibrotic Process.Biomolecules · 2026Review
- Neutrophil Heterogeneity after Myocardial Infarction.Journal of innate immunity · 2026Review
- Integrated multi-omics profiling of the early post-infarct heart reveals a hub gene network associated with myeloid-driven inflammation.Frontiers in cardiovascular medicine · 2026Article
- Immune checkpoint inhibitors and cardiovascular toxicity: immunology, pathophysiology, diagnosis, and management.Journal of thrombosis and thrombolysis · 2025Review
- Cardioprotective effects of the extracellular chaperone clusterin in acute myocardial infarction.European journal of clinical investigation · 2025Article
- Short-term S100A8/A9 Blockade Promotes Cardiac Neovascularization after Myocardial Infarction.Journal of cardiovascular translational research · 2024Article
- The Role of Alarmins in the Pathogenesis of Atherosclerosis and Myocardial Infarction.Current issues in molecular biology · 2024Review
- Macrophage heterogeneity in myocardial infarction: Evolution and implications for diverse therapeutic approaches.iScience · 2024Review
- Repair of the Infarcted Heart: Cellular Effectors, Molecular Mechanisms and Therapeutic Opportunities.Circulation research · 2024Review
- Extracellular vesicles from dental pulp mesenchymal stem cells modulate macrophage phenotype during acute and chronic cardiac inflammation in athymic nude rats with myocardial infarction.Inflammation and regeneration · 2024Article
- IL-6 and IL-10 Levels in Rats Blood Plasma as Immune Responses Post Radioiodine (I-131) Administration.Asian Pacific journal of cancer prevention : APJCP · 2024Article
- Relationship between cathepsins and cardiovascular diseases: a Mendelian randomized study.Frontiers in pharmacology · 2024Article
- Smartphone-Aided Fluorescence Detection of Cardiac Biomarker Myoglobin by a Ratiometric Fluorescent AuNCs-QDs Nanohybrids Probe with High Sensitivity.Journal of fluorescence · 2024Article
- Hepatic SPARC Expression Is Associated with Inflammasome Activation during the Progression of Non-Alcoholic Fatty Liver Disease in Both Mice and Morbidly Obese Patients.International journal of molecular sciences · 2023Article
- Don't go breakin' my heart: cardioprotective alterations to the mechanical and structural properties of reperfused myocardium during post-infarction inflammation.Biophysical reviews · 2023Review
- Molecular and cellular pathophysiology of circulating cardiomyocyte-specific cell free DNA (cfDNA): Biomarkers of heart failure and potential therapeutic targets.Genes & diseases · 2023Review
- Immune cells drive new immunomodulatory therapies for myocardial infarction: From basic to clinical translation.Frontiers in immunology · 2023Review
- Inflammation, dysregulated iron metabolism, and cardiovascular disease.Frontiers in aging · 2023Review
18 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
4 authors at 1 institution in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
During myocardial infarction, sterile inflammation occurs. The danger model is a solid theoretic framework that explains this inflammation as danger associated molecular patterns activate the immune system. The innate immune system can sense danger signals through different pathogen recognition receptors (PRR) such as toll-like receptors, nod-like receptors and receptors for advanced glycation endproducts. Activation of a PRR results in the production of cytokines and the recruitment of leukocytes to the site of injury. Due to tissue damage and necrosis of cardiac cells, danger signals such as extracellular matrix (ECM) breakdown products, mitochondrial DNA, heat shock proteins and high mobility box 1 are released. Matricellular proteins are non-structural proteins expressed in the ECM and are upregulated upon injury. Some members of the matricellular protein family (like tenascin-C, osteopontin, CCN1 and the galectins) have been implicated in the inflammatory and reparative responses following myocardial infarction and may function as danger signals. In a clinical setting, danger signals can function as prognostic and/or diagnostic biomarkers and for drug targeting. In this review we will provide an overview of the established knowledge on the role of danger signals in myocardial infarction and we will discuss areas of interest for future research.
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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.