Key result
Plasmin and tPA may drive blood-brain barrier disruption during thrombolysis for ischemic stroke.
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Plasmin, the principal downstream product of tissue-type plasminogen activator (tPA), is known for its potent fibrin-degrading capacity but is also recognized for many non-fibrinolytic activities. Curiously, plasmin has not been conclusively linked to blood-brain barrier (BBB) disruption during recombinant tPA (rtPA)-induced thrombolysis in ischemic stroke. This is surprising given the substantial involvement of tPA in the modulation of BBB permeability and the co-existence of tPA and plasminogen in both blood and brain throughout the ischemic event. Here, we review the work that argues a role for plasmin together with endogenous tPA or rtPA in BBB alteration, presenting the overall controversy around the topic yet creating a rational case for an involvement of plasmin in this process.
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Niego et al. (2014) conducted a review in Ischemic stroke. Plasmin and tissue-type plasminogen activator (tPA/rtPA) was evaluated on Blood-brain barrier (BBB) alteration/disruption. Plasmin alongside endogenous or recombinant tPA may play a role in blood-brain barrier alteration during thrombolysis in ischemic stroke.
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