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CD47 信号转导通路在血管疾病中的最新进展。

Recent Advancements in CD47 Signal Transduction Pathways Involved in Vascular Diseases.

机构信息

Department of Neurology, The First Hospital of Jilin University, Changchun 130021, China.

出版信息

Biomed Res Int. 2020 Jul 15;2020:4749135. doi: 10.1155/2020/4749135. eCollection 2020.

DOI:10.1155/2020/4749135
PMID:32733941
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7378613/
Abstract

Cardiovascular and cerebrovascular diseases caused by atherosclerosis have a high disability rate and reduce the quality of life of the population. Therefore, understanding the mechanism of atherosclerosis and its control may interfere with the progression of atherosclerosis and thus control the occurrence of diseases closely related to atherosclerosis. TSP-1 is a factor that has been found to have an antiangiogenic effect, and CD47, as the receptor of TSP-1, can participate in the regulation of antiangiogenesis of atherosclerosis. VEGF is an important regulator of angiogenesis, and TSP-1/CD47 can cause VEGF and its downstream expression. Therefore, the TSP-1/CD47/VEGF/VEGFR2 signal may have an important influence on atherosclerosis. In addition, some inflammatory factors, such as IL-1 and NLRP3, can also affect atherosclerosis. This review will be expounded focusing on the pathogenesis and influencing factors of atherosclerosis.

摘要

由动脉粥样硬化引起的心血管和脑血管疾病具有高致残率,并降低了人群的生活质量。因此,了解动脉粥样硬化的机制及其控制可能会干扰动脉粥样硬化的进展,从而控制与动脉粥样硬化密切相关的疾病的发生。TSP-1 是一种已被发现具有抗血管生成作用的因子,而 CD47 作为 TSP-1 的受体,可以参与动脉粥样硬化的抗血管生成调节。VEGF 是血管生成的重要调节剂,TSP-1/CD47 可以引起 VEGF 及其下游表达。因此,TSP-1/CD47/VEGF/VEGFR2 信号可能对动脉粥样硬化有重要影响。此外,一些炎症因子,如 IL-1 和 NLRP3,也可以影响动脉粥样硬化。本综述将重点阐述动脉粥样硬化的发病机制和影响因素。

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Blocking CD47 efficiently potentiated therapeutic effects of anti-angiogenic therapy in non-small cell lung cancer.阻断 CD47 可有效增强抗血管生成治疗在非小细胞肺癌中的疗效。
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Anti-inflammatory cytokines IL-35 and IL-10 block atherogenic lysophosphatidylcholine-induced, mitochondrial ROS-mediated innate immune activation, but spare innate immune memory signature in endothelial cells.抗炎细胞因子 IL-35 和 IL-10 阻断动脉粥样硬化性溶血磷脂酰胆碱诱导的、线粒体 ROS 介导的固有免疫激活,但在血管内皮细胞中保留固有免疫记忆特征。
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