ReviewFrontiers in immunology2025
The alarmin tandem: unraveling the complex effect of S100A8/A9 - from atherosclerosis to cardiac arrhythmias.
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 17 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
17 citing papers in PubMed.
- S100A8/A9 and S100A12 Proteins and Macrophage Polarization: Therapeutic Targets in Atherosclerosis.Biomolecules · 2026Review
- Research progress on coronary heart disease and cytokines: mechanisms, clinical implications, and future directions.Journal of cardiothoracic surgery · 2026Review
- Beyond Reperfusion: Early Molecular Drivers and Therapeutic Opportunities in Acute Post-Infarction Cardiac Fibrosis.International journal of molecular sciences · 2026Review
- Association of Serum Calprotectin and the C-Reactive Protein-Triglyceride-Glucose Index with SYNTAX Score in Patients with Newly Diagnosed Coronary Artery Disease.Medicina (Kaunas, Lithuania) · 2026Article
- Compartment-specific soluble immune profiles associated with preterm birth, perinatal death, and low birthweight in pregnant individuals living with HIV.bioRxiv : the preprint server for biology · 2026Article
- Immunometabolism in Cardiac Remodeling: Mechanisms and Therapeutic Perspectives.International journal of molecular sciences · 2026Review
- Neoplastic Disorders and Cardiovascular Comorbidities in Geriatric Patients: A Simple Association?Geriatrics (Basel, Switzerland) · 2026Review
- Mechanisms of Cardiac Inflammation in Heart Failure: Role of Dietary Patterns, Nutrients, and Therapeutic Strategies.Nutrients · 2026Review
- Atherogenic Lipoprotein Burden, Metabolic Stress and Immune Activation Associated with Coronary Atherosclerosis in Patients with Psoriasis.International journal of molecular sciences · 2026Article
- Integrating Network Toxicology, Machine Learning, and Molecular Dynamics to Explore the Molecular Network of Triclosan-Induced Acute Myocardial Infarction.International journal of molecular sciences · 2026Article
- Myocardial Ischemia-Reperfusion Injury-Mechanistic Insights and Novel Therapeutics.International journal of molecular sciences · 2026Review
- Activation of the S100A8/A9 Alarmin Amplifies Inflammatory Pathways in Equine Ascending Placentitis.International journal of molecular sciences · 2026Article
- Oxidative Stress, Mitochondrial Homeostasis, and Sirtuins in Atrial Fibrillation.International journal of molecular sciences · 2025Review
- Mitochondrial Quality Control and Cell Death.International journal of molecular sciences · 2025Review
- Evolution in the Diagnosis and Treatment of Myocarditis in Recent Years: State of the Art.Journal of clinical medicine · 2025Review
- From Tissue to Transcriptome: A Systematic Review of Multi-Level Evidence for Immune Dysregulation in Atrial Fibrillation.Journal of clinical medicine · 2025Review
- Oxidative Stress, Mitochondrial Quality Control, Autophagy, and Sirtuins in Heart Failure.International journal of molecular sciences · 2025Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Introduction: Inflammation plays a crucial role in the pathophysiology of cardiovascular diseases (CVDs), particularly in heart failure (HF), cardiac arrhythmias, and atherosclerotic cardiovascular disease (ASCVD). The calcium-binding proteins S100A8 and S100A9, primarily functioning as a heterodimer (S100A8/A9), have emerged as essential mediators in cardiovascular pathophysiology through the toll-like receptor 4 (TLR-4) and receptor for advanced glycation end-products (RAGE) signaling pathway. This review aims to comprehensively explore the role of S100A8/A9 in ASCVD, HF, and cardiac arrhythmogenesis, and to discuss its pathophysiological implications, clinical significance, and potential utility as a novel therapeutic target. Main text: In ASCVD, S100A8/A9 promotes endothelial dysfunction and facilitates monocyte recruitment and foam cell formation. The heterodimer amplifies vascular inflammation Conclusion: S100A8/A9 plays a critical dual role in cardiovascular inflammation and repair, emerging not only as a biomarker but also as a promising therapeutic target in ASCVD, HF, and cardiac arrhythmogenesis, with potential applications for anti-inflammatory intervention. However, further research is needed to elucidate the precise mechanisms linking S100A8/A9 and CVDs and to validate therapeutic interventions targeting this pathway.
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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.