CFTR Therapeutics Normalize Cerebral Perfusion Deficits in Mouse Models of Heart Failure and Subarachnoid Hemorrhage

•The cystic fibrosis transmembrane conductance regulator (CFTR) is a significant modulator of cerebrovascular reactivity; the loss of CFTR function enhances myogenic vasoconstriction.•Heart failure and subarachnoid hemorrhage downregulate cerebrovascular CFTR protein expression; this leads to enhanced cerebral artery vasoconstriction, reduced cerebral perfusion, neuronal injury, and ultimately, neurologic deficits.•CFTR therapeutics that maintain CFTR expression normalize the perfusion deficits, reduce neuronal injury, and improve neurologic function in these pathological settings.