In the acute ischemic phase, HMGB1 protein contributes to thromboinflammation, blood–brain barrier disruption, and immune cell activation, amplifying tissue injury. Its interaction with thrombolytic therapies further promotes MMP9 activity, increasing the risk of hemorrhagic transformation.
Beyond the acute phase, HMGB1 also participates in neurovascular remodeling and recovery, underscoring its dual and context-dependent role.
Mechanistically, HMGB1 regulates macrophage and microglial polarization, neutrophil extracellular trap formation, excitotoxicity, and autophagic pathways. Its systemic effects extend to post-stroke complications, including immunosuppression and neuropsychiatric outcomes.
HMGB1 represents both a promising therapeutic target and a prognostic biomarker in stroke management. Targeting HMGB1 signaling pathways may support the development of neuroprotective strategies, reduce post-ischemic inflammation, and potentially expand the therapeutic window for thrombolysis.
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