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急性冠状动脉综合征中的促炎细胞因子。

Pro-inflammatory Cytokines in Acute Coronary Syndromes.

机构信息

1st Department of Cardiology, 'Hippokration' Hospital, National and Kapodistrian University of Athens Medical School, Athens, Greece.

出版信息

Curr Pharm Des. 2020;26(36):4624-4647. doi: 10.2174/1381612826666200413082353.

DOI:10.2174/1381612826666200413082353
PMID:32282296
Abstract

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-α) 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-α 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-γ, 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.

摘要

背景

在过去的几十年中,炎症和免疫系统激活在冠状动脉疾病(CAD)的发生和进展中的作用已经确立。

目的

本研究旨在阐述细胞因子及其在 ACS 发生前后的作用之间的相互作用。

方法

我们系统地在 MEDLINE、COCHRANE 和 EMBASE 数据库中搜索了与炎症、细胞因子、易损斑块和心肌梗死相关的最相关文章。

结果

不同类别的细胞因子(白细胞介素[IL]-1 家族、肿瘤坏死因子-α(TNF-α)家族、趋化因子、脂肪因子、干扰素)参与导致动脉粥样硬化斑块不稳定的整个过程,从而导致心肌梗死的发生。特别是 IL-1 和 TNF-α 家族参与炎症细胞积聚、易损斑块形成、血小板聚集、心肌细胞凋亡和心肌梗死后的不良重构。一些细胞因子,如 IL-6、脂联素、干扰素-γ,在 ACS 患者中具有显著的预后价值。因此,研究重点关注 ACS 中的炎症调节,以改善临床结果。

结论

了解伴随每种细胞因子-细胞因子受体相互作用的独特特征可以阐明参与斑块不稳定的信号通路,并为改善 ACS 患者的心血管预后提供未来的治疗策略。

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