ReviewCells2025
Inflammatory Mechanisms in Acute Coronary Syndromes: From Pathophysiology to Therapeutic Targets.
Review in Cells, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers, 1 of them a synthesis 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
10 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Cardiovascular Benefit and Gastrointestinal Risk of Colchicine in Secondary Prevention: Risk Associated with Dose and Treatment Duration.American journal of cardiovascular drugs : drugs, devices, and other interventions · 2026Pooled it
- Taoren Honghua Jian Regulate NLRP3 Inflammasome of Coronary Artery Disease Patients: A Multi-Center, Double-Blind, Randomized Controlled Trial.Vascular health and risk management · 2026Trial
- Subclinical Atherosclerosis, Hyperlipidemia and New-Onset Diabetes Should Not Be Ignored Despite Initial Angiographic Exclusion of Significant Atherosclerotic Occlusive Arterial Disease.Diagnostics (Basel, Switzerland) · 2026Article
- Prognostic Value of the Osaka Prognostic Score for One-Year Mortality in Patients with ST-Segment Elevation Myocardial Infarction: A Retrospective Observational Cohort Study.Journal of clinical medicine · 2026Article
- Vericiguat in the Post-Stabilization Phase of HFrEF: Targeting Residual Risk Across the Ischemia-Decompensation Continuum.International journal of molecular sciences · 2026Review
- Advances in the Diagnosis and Management of Acute Coronary Syndrome: A Clinical Review.Cureus · 2026Review
- Anti-Inflammatory Therapies in Acute Coronary Syndromes-A Review of Immunological, Genetic, and Clinical Challenges for Precision Medicine.Journal of clinical medicine · 2026Review
- Developmental Programming of Drug Response: Microbiota as a Missing Dimension in Perinatal Drug Discovery.International journal of molecular sciences · 2026Review
- Incident Heart Failure Risk Following COVID-19 Recovery: A Systematic Review and Meta-Analysis.Journal of clinical medicine · 2026Review
- SASP-mediated cellular senescence following myocardial infarction: from spatiotemporal immune regulation to therapeutic strategies.Frontiers in immunology · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Inflammation plays a pivotal role in the pathogenesis of acute coronary syndromes (ACS), contributing to plaque instability, thrombosis, and myocardial injury. This review aims to comprehensively examine the inflammatory mechanisms underlying ACS and evaluate current and emerging anti-inflammatory therapeutic strategies. We conducted a comprehensive literature review examining the role of inflammatory pathways in ACS pathophysiology, including innate and adaptive immune responses, key inflammatory mediators, and cellular mechanisms. We analyzed current evidence for anti-inflammatory therapies and their clinical outcomes in ACS management. Inflammatory processes in ACS involve complex interactions between innate immune cells (neutrophils, macrophages, monocytes) and adaptive immune cells (T lymphocytes, B cells). Key mechanisms include neutrophil extracellular trap (NET) formation, macrophage polarization, T cell subset imbalances (Th1/Th17 predominance with regulatory T cell dysfunction), and complement activation. Inflammatory biomarkers such as C-reactive protein, interleukin-6, and NET-specific markers demonstrate prognostic value. Anti-inflammatory therapies including colchicine, canakinumab (IL-1β inhibition), and methotrexate have shown cardiovascular benefits in clinical trials. Emerging targets include NET inhibition, T cell modulation, and precision inflammatory profiling approaches. Inflammation represents a critical therapeutic target in ACS beyond traditional risk factor modification. While colchicine and IL-1β inhibition have demonstrated clinical efficacy, future strategies should focus on precision medicine approaches targeting specific inflammatory pathways based on individual patient profiles. Integration of anti-inflammatory therapy with lipid management and antithrombotic strategies offers promise for improving ACS outcomes through comprehensive targeting of the multifactorial pathophysiology underlying coronary artery disease.
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Identifiers
What Socratic 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 Socratic graph.