Topic: Plasma kallikrein

Clinical intervention for ischemic stroke patients is limited to the acute phase, leaving ~80% of stroke patients without effective pharmacological intervention and unsatisfactory neurological outcome. Therefore, subacute therapeutics that resolve thrombosis and inflammatory processes to support tissue recovery are urgently in need. Plasma kallikrein (PK), a member of the kallikrein-kinin-system, promotes vascular damage, inflammation, and thrombosis. We hypothesize that prolonged PK activation determines stroke severity and impairs tissue recovery. Thus, wild-type mice were subjected to 60 mi