神秘之网:揭示肠道-微生物-免疫-心脏轴中的 NETosis 在急性心肌梗死和心力衰竭中的作用。

IF 1.3 Q3 CARDIAC & CARDIOVASCULAR SYSTEMS Cardiovascular Endocrinology & Metabolism Pub Date : 2024-08-08 eCollection Date: 2024-09-01 DOI:10.1097/XCE.0000000000000309
Tai Yasuda, Kate Deans, Aditi Shankar, Robert Chilton
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引用次数: 0

摘要

本综述概述了急性心肌梗死(AMI)和心力衰竭中嗜中性粒细胞胞外捕获物(NET)的作用及其与肠道微生物组的相互作用。嗜中性粒细胞胞外捕获物(NET)的释放及其与肠道微生物组在急性心肌梗塞(AMI)和心力衰竭中的相互作用。炎症和饮食因素可激活 NETosis,这表明它与代谢状况有关。在心力衰竭的病例中,NETosis受炎症分子(如C反应蛋白(CRP)、克鲁珀类因子2(KLF2)--一种在控制炎症中发挥作用的蛋白质)和血管紧张素II的调节。肠道微生物组的变化与急性心肌梗死后心脏损伤的严重程度和恢复以及心力衰竭的进展有关。微生物组的影响延伸到免疫调节和炎症反应,可能会影响 NETosis。
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The web of intrigue: unraveling the role of NETosis within the gut-microbiome-immune-heart axis in acute myocardial infarction and heart failure.

This review summarizes the role of NETosis, or the release of neutrophil extracellular traps (NETs), and its interplay with the gut microbiome in acute myocardial infarction (AMI) and heart failure. NETosis contributes to inflammation, thrombosis, and atherothrombosis, all central to the pathophysiology of AMI and heart failure. NETosis can be activated by inflammation and dietary factors, indicating association with metabolic conditions. In cases of heart failure, NETosis is regulated by inflammatory molecules such as C-reactive protein (CRP), and Krüppel-like factor 2 (KLF2) - a protein that plays a role in controlling inflammation, and angiotensin II. Changes in the gut microbiome are linked to the severity and recovery of cardiac injury post-AMI and heart failure progression. The microbiome's influence extends to immune modulation and inflammatory responses, potentially affecting NETosis.

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来源期刊
Cardiovascular Endocrinology & Metabolism
Cardiovascular Endocrinology & Metabolism CARDIAC & CARDIOVASCULAR SYSTEMS-
CiteScore
5.60
自引率
0.00%
发文量
24
期刊最新文献
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