Formyl peptide receptor 1 signaling exacerbates hemorrhagic transformation following tPA thrombolysis in mice.
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ABSTRACT: Hemorrhagic transformation (HT) is a severe complication occurring in ischemic stroke patients undergoing tPA thrombolytic therapy, which significantly limits its clinical applicability. The mechanism and intervention of HT is still not fully understood. In our study, we found that an increased mobilization of circulating formyl peptide receptor 1 (FPR1) expressing leucocytes into the ischemic brain after tPA treatment in mice. In Fpr1-/- mice, neutrophil mobilization and HT occurrence after tPA thrombolysis decreased. Notably, pharmacological inhibition of FPR1 using a novel antagonist T0080 effectively mitigated tPA-associated HT, concurrently reducing neutrophil infiltration into the brain and preserving blood-brain barrier (BBB) integrity. We further revealed that bra
SUBMITTER: Lv J
PROVIDER: S-EPMC12597790 | biostudies-literature | 2025 Nov
REPOSITORIES: biostudies-literature
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