Yasuda Tai, Deans Kate, Shankar Aditi, Chilton Robert
Department of Anesthesiology, University Hospital, UTHSC San Antonio.
Department of Cardiology, South Texas Department of Veteran Affairs.
Cardiovasc Endocrinol Metab. 2024 Aug 8;13(3):e0309. doi: 10.1097/XCE.0000000000000309. eCollection 2024 Sep.
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.
本综述总结了中性粒细胞胞外诱捕网形成(NETosis),即中性粒细胞胞外陷阱(NETs)的释放,及其在急性心肌梗死(AMI)和心力衰竭中与肠道微生物群的相互作用。NETosis会导致炎症、血栓形成和动脉粥样硬化血栓形成,这些都是AMI和心力衰竭病理生理学的核心。NETosis可由炎症和饮食因素激活,表明其与代谢状况有关。在心力衰竭病例中,NETosis受炎症分子如C反应蛋白(CRP)和Krüppel样因子2(KLF2,一种在控制炎症中起作用的蛋白质)以及血管紧张素II的调节。肠道微生物群的变化与AMI后心脏损伤的严重程度和恢复以及心力衰竭进展有关。微生物群的影响延伸至免疫调节和炎症反应,可能影响NETosis。