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Gut microbiota aggravate cardiac ischemia-reperfusion injury via regulating the formation of neutrophils extracellular traps
Myocardial infarction (MI) is a leading cause of death worldwide for which there is no cure. Percutaneous coronary intervention (PCI) can restore blood supply in a timely manner, which greatly reduces the mortality of patients, but ischemia/reperfusion (I/R) injury is inevitable. A number of clinica...
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Published in: | Life sciences (1973) 2022-08, Vol.303, p.120670-120670, Article 120670 |
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Main Authors: | , , , , |
Format: | Article |
Language: | English |
Subjects: | |
Citations: | Items that this one cites Items that cite this one |
Online Access: | Get full text |
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Summary: | Myocardial infarction (MI) is a leading cause of death worldwide for which there is no cure. Percutaneous coronary intervention (PCI) can restore blood supply in a timely manner, which greatly reduces the mortality of patients, but ischemia/reperfusion (I/R) injury is inevitable. A number of clinical studies have shown that gut microbiota play an essential role in cardiovascular diseases. This study aims to explore the mechanism of gut microbiota to limit I/R injury.
This study adopted the myocardial I/R model using gut microbiota clearance mice, neutrophil clearance mice and double-scavenging mice, and explored the relationship between gut microbiota and NETs during I/R injury. Neutrophils were isolated in vitro to explore the effect of NETs on myocardial cell injury and its molecular mechanism.
Gut microbiota aggravate cardiac I/R injury via regulating the formation of NETs. The migration of gut microbiota to blood stimulated the formation of NETs after cardiac I/R. NETs, which can directly lead to apoptosis of myocardial cells and myocardial microvascular endothelial cells. The time point of NETs formation in tissue and blood after I/R were determined by experiments.
It was confirmed that gut microbiota participates in cardiac I/R injury by regulating the formation of NETs, which reveals a new mechanism of I/R injury and provides a new potential target for the treatment of I/R injury. |
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ISSN: | 0024-3205 1879-0631 |
DOI: | 10.1016/j.lfs.2022.120670 |