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These findings collectively emphasize that gut dysbiosis, increased intestinal permeability, and even gutlung microbial translocation can amplify neuroinflammation and worsen ischemic stroke outcomes, underscoring the need to consider the gutbrainlung axis as a potential target for improving stroke prognosis

Direct neuronal protection by the proteaseactivated receptor PAR4 antagonist ML354 after experimental stroke in mice

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A conserved PLPLRT/SD motif of STING mediates the recruitment and activation of TBK1

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