ReviewJournal of molecular and cellular cardiology2016
The crossroads of inflammation, fibrosis, and arrhythmia following myocardial infarction.
Review in Journal of molecular and cellular cardiology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT05112731 (Action of Glycation and Inflammation in Operative Ischemic Heart Disease), which is not on this map. Cited by 145 papers, 2 of them syntheses 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.
Action of Glycation and Inflammation in Operative Ischemic Heart Disease
Who cites it
145 citing papers in PubMed, 2 syntheses or guidelines pooled it.
- Clinical evidence-guided network pharmacology analysis reveals a critical contribution of β1-adrenoreceptor upregulation to bradycardia alleviation by Shenxian-Shengmai.BMC complementary and alternative medicine · 2019Pooled it
- Guidelines for experimental models of myocardial ischemia and infarction.American journal of physiology. Heart and circulatory physiology · 2018Guideline
- Influence of the Residual Gensini Score on Prognosis of Patients With ST-Elevation Myocardial Infarction.Catheterization and cardiovascular interventions : official journal of the Society for Cardiac Angiography & Interventions · 2026Observational
- Prioritizing Discovery and Advancements in Arrhythmia Therapies: NIH/NHLBI Workshop.JACC. Clinical electrophysiology · 2026Review
- Beyond Reperfusion: Early Molecular Drivers and Therapeutic Opportunities in Acute Post-Infarction Cardiac Fibrosis.International journal of molecular sciences · 2026Review
- Myocardial Fibrosis in Cardiovascular Disease: An Integrative Biomarker-Imaging Framework Linking Molecular Mechanisms to Structural Phenotypes.Journal of clinical medicine · 2026Review
- Article
- Local to Systemic Inflammation-From Generation to Prognosis in Acute Coronary Syndrome.Biomedicines · 2026Review
- Cellular and molecular signals of cardiac wound healing after myocardial infarction.American journal of physiology. Heart and circulatory physiology · 2026Review
- More Than a Cleanup Crew: The Expanding Biology of Efferocytosis.Arteriosclerosis, thrombosis, and vascular biology · 2026Review
- Chemogenetic activation of cholinergic intrinsic cardiac ganglia improves border zone oxygenation and reduces arrhythmias during acute local ischemia.Frontiers in cardiovascular medicine · 2026Article
- High Burden of Premature Ventricular Contractions Upregulates Transcriptional Markers of Inflammation and Promotes Adverse Cardiac Remodeling Linked to Cardiomyopathy.Circulation. Arrhythmia and electrophysiology · 2026Article
- MiRNA Regulations in Cardiotoxicity Induced by Oncologic Therapies and Possible Immune Response.Current medicinal chemistry · 2026Review
- The core mechanism of traditional Chinese medicine in improving myocardial fibrosis: restoring the dynamic balance of mitochondrial quality control.Frontiers in cardiovascular medicine · 2026Review
- Cardiac resident macrophages: the emerging role in arrhythmogenesis.Frontiers in immunology · 2026Review
- From tumor immunotherapy to myocardial injury: A mechanistic discussion of immune checkpoint inhibitor‑related myocarditis (Review).Molecular medicine reports · 2025Review
- Review
- A Macrophage-Derived Factor on Human iPSC-Derived Cardiomyocyte Function: The Role of Osteopontin.Cells · 2025Article
- Sonogenetic neuromodulation prevents post-myocardial infarction malignant arrhythmia and cardiac remodeling through the brain-heart circuit.Basic research in cardiology · 2025Article
- Resistin-like molecule γ attacks cardiomyocyte membranes and promotes ventricular tachycardia.Science (New York, N.Y.) · 2025Article
85 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.
Funding
Abstract
Optimal healing of damaged tissue following myocardial infarction (MI) requires a coordinated cellular response that can be divided into three phases: inflammatory, proliferative/reparative, and maturation. The inflammatory phase, characterized by rapid influx of cytokines, chemokines, and immune cells, is critical to the removal of damaged tissue. The onset of the proliferative/reparative phase is marked by increased proliferation of myofibroblasts and secretion of collagen to replace dead tissue. Lastly, crosslinking of collagen fibers and apoptosis of immune cells marks the maturation phase. Excessive inflammation or fibrosis has been linked to increased incidence of arrhythmia and other MI-related pathologies. This review describes the roles of inflammation and fibrosis in arrhythmogenesis and prospective therapies for anti-arrhythmic treatment.
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Identifiers
What OpenQuestion holds
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.