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Pro-inflammatory Cytokines in Acute Coronary Syndromes

Journal

CURRENT PHARMACEUTICAL DESIGN
Volume 26, Issue 36, Pages 4624-4647

Publisher

BENTHAM SCIENCE PUBL LTD
DOI: 10.2174/1381612826666200413082353

Keywords

Acute coronary syndrome; atherosclerosis; inflammation; cytokines; adipokines; vulnerable plaque

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Background: Over the last decades, the role of inflammation and immune system activation in the initiation and progression of coronary artery disease (CAD) has been established. Objectives: The study aimed to present the interplay between cytokines and their actions preceding and shortly after ACS. Methods: We searched in a systemic manner the most relevant articles to the topic of inflammation, cytokines, vulnerable plaque and myocardial infarction in MEDLINE, COCHRANE and EMBASE databases. Results: Different classes of cytokines (intereleukin [IL]-1 family, Tumor necrosis factor-alpha (TNF-alpha) family, chemokines, adipokines, interferons) are implicated in the entire process leading to destabilization of the atherosclerotic plaque, and consequently, to the incidence of myocardial infarction. Especially IL-1 and TNF-alpha family are involved in inflammatory cell accumulation, vulnerable plaque formation, platelet aggregation, cardiomyocyte apoptosis and adverse remodeling following the myocardial infarction. Several cytokines such as IL-6, adiponectin, interferon-gamma, appear with significant prognostic value in ACS patients. Thus, research interest focuses on the modulation of inflammation in ACS to improve clinical outcomes. Conclusion: Understanding the unique characteristics that accompany each cytokine-cytokine receptor interaction could illuminate the signaling pathways involved in plaque destabilization and indicate future treatment strategies to improve cardiovascular prognosis in ACS patients.

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