ReviewCurrent atherosclerosis reports2026
Role of Interleukin-6 in Atherothrombosis and Myocardial Infarction.
Review in Current atherosclerosis reports, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 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.
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Who cites it
5 citing papers in PubMed.
- Cross-Species Identification and Validation of Hub Genes and Potential Therapeutic Targets in Myocardial Infarction.International journal of molecular sciences · 2026Article
- Immunothrombotic Cell-Cell Communication Networks in Coronary Atherosclerosis: Critical Insights from Single-Cell and Spatial Systems Biology.International journal of molecular sciences · 2026Review
- Serotonin 5-HT7 receptor signaling modulates inflammatory responses and survival after myocardial infarction.Journal of translational medicine · 2026Article
- Review
- Bisphenols-enhanced platelet aggregation via TP, P2YFrontiers in pharmacology · 2026Article
Corrections and comments
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Authors and funding
9 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
purpose of the reviewWe aimed to summarize the pathogenic role of IL-6 in atherothrombosis and myocardial infarction (MI), with focus on novel pathogenic mechanisms and current IL-6 targeted therapy in clinical cohorts. RECENT
findingsIL-6 plays a major role in the pathogenesis of cardiovascular disease interacting with aging- and metabolic-driven inflammation, two conditions with overlapping molecular mechanisms. A novel pathogenic mechanism in cardiovascular disease (CVD) is the interaction between IL-6 and clonal hematopoiesis of indeterminate potential, CHIP, that involve the ten-eleven translocation-2 gene, a molecule with role in epigenetics. Recent studies showed reduced inflammation, a reduction in Lp (a) and inhibitory effects on platelets by anti-IL-6 (ziltivekimab) therapy in patients at risk for CVD. Anti-IL-6 receptor therapy (tocilizumab) showed reduced inflammation and improved myocardial function in MI patients, involving reduced degranulation in neutrophils and modulation of monocytes. Studies with clinical endpoints are still lacking and there also a need for developing therapy that selectively block the harmful IL-6 trans-signaling. IL-6 plays an important and many-faceted role in atherothrombosis including MI and ischemic stroke, and the IL-6 system represent a promising but still evolving therapeutic approach. A comprehensive understanding of the complexity of IL-6 signaling is needed to improve such treatment strategies.
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Registered trials
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