Abstract
The successful clinical treatment of acute ischemic stroke pivots on reestablishing blood flow. After attempting recanalization, the “no-reflow” phenomenon undermines the long-term benefits of clot-busting strategies, including thrombolytic and intravascular thrombectomy. A key pathological driver of this phenomenon is immunothrombosis, a specialized form of microthrombosis characterized by the aberrant aggregation of platelets with neutrophils and subsequent microvascular clot formation. The immunothrombotic process may be initiated or promoted by brain ischemia-induced endothelial inflammation. In this commentary, we elaborate on the mechanisms underlying the role of endothelial inflammation in the no-reflow cascade, and we recommend targeting immunothrombosis to mitigate no-reflow and optimize stroke management.
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