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白细胞介素 17,动脉粥样硬化的双刃剑。

Interleukin 17, the double-edged sword in atherosclerosis.

机构信息

School of Medicine, Tehran University of Medical Sciences, Tehran, Iran; Cancer Immunology Project (CIP), Universal Scientific Education and Research Network (USERN), Tehran, Iran.

Cancer Immunology Project (CIP), Universal Scientific Education and Research Network (USERN), Tehran, Iran; School of Medicine, Iran University of Medical Sciences, Tehran, Iran; Network of Immunity in Infection, Malignancy and Autoimmunity (NIIMA), Universal Scientific Education and Research Network (USERN), Tehran, Iran.

出版信息

Immunobiology. 2022 May;227(3):152220. doi: 10.1016/j.imbio.2022.152220. Epub 2022 Apr 18.

DOI:10.1016/j.imbio.2022.152220
PMID:35452921
Abstract

Cardiovascular diseases, including atherosclerosis, are the number one cause of death worldwide. These diseases have taken the place of pneumonia and other infectious diseases in the epidemiological charts. Thus, their importance should not be underestimated. Atherosclerosis is an inflammatory disease. Therefore, immunological signaling molecules and immune cells carry out a central role in its etiology. One of these signaling molecules is interleukin (IL)-17. This relatively newly discovered signaling molecule might have a dual role as acting both pro-atherogenic and anti-atherogenic depending on the situation. The majority of articles have discussed IL-17 and its action in atherosclerosis, and it may be a new target for the treatment of patients with this disease. In this review, the immunological basis of atherosclerosis with an emphasis on the role of IL-17 and a brief explanation of the role of IL-17 on atherosclerogenic disorders will be discussed.

摘要

心血管疾病,包括动脉粥样硬化,是全球头号死因。这些疾病在流行病学图表中已经取代了肺炎和其他传染病。因此,它们的重要性不容低估。动脉粥样硬化是一种炎症性疾病。因此,免疫信号分子和免疫细胞在其发病机制中发挥着核心作用。其中一种信号分子是白细胞介素(IL)-17。这种相对较新发现的信号分子可能具有双重作用,即具有促动脉粥样硬化和抗动脉粥样硬化作用,具体取决于情况。大多数文章都讨论了 IL-17 及其在动脉粥样硬化中的作用,它可能是治疗这种疾病患者的一个新靶点。在这篇综述中,我们将讨论动脉粥样硬化的免疫学基础,重点介绍 IL-17 的作用,并简要解释 IL-17 在动脉粥样硬化性疾病中的作用。

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Front Immunol. 2025 Jan 29;16:1461535. doi: 10.3389/fimmu.2025.1461535. eCollection 2025.
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