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Contribution of NETs to IS. After forming in blood vessels, NETs can cause blood-brain barrier damage, which may be related to the granular protein it contains. Intravascular NETs can enhance coagulation activity and act as assembly platform to promote thrombosis. After transferring to brain parenchyma by changing phenotype, neutrophils release NETs, which can directly damage neurons through cytotoxic proteins or aggravate neuroinflammation by activating inflammatory cells.
