title: Mechanisms of neurovascular dysfunction in acute ischemic brain.
abstract: The neurovascular unit is now well accepted as a conceptual framework for investigating the mechanisms of ischemic stroke. From a molecular and cellular perspective, three broad mechanisms may underlie stroke pathophysiology--excitotoxicity, oxidative stress and inflammation. To date, however, most investigations of these basic mechanisms have focused on neuronal responses. In this mini-review, we ask whether these mechanisms of excitotoxicity, oxidative stress and inflammation can also be examined in terms of non-neuronal interactions in the neurovascular unit, including the release of extracellular vesicles for cell-cell signaling.
authors.forename: Y
authors.initials: Y
authors.lastname: Terasaki
authors.forename: Y
authors.initials: Y
authors.lastname: Liu
authors.forename: K
authors.initials: K
authors.lastname: Hayakawa
authors.forename: L D
authors.initials: LD
authors.lastname: Pham
authors.forename: E H
authors.initials: EH
authors.lastname: Lo
authors.forename: X
authors.initials: X
authors.lastname: Ji
authors.affiliation: Neuroprotection Research Laboratory, Departments of Radiology and Neurology, Massachusetts General Hospital and Harvard Medical School, USA. karai@partners.org.
authors.forename: K
authors.initials: K
authors.lastname: Arai
mesh_terms: D000818:Animals; D002545:Brain Ischemia / Q000378:metabolism / Q000503:physiopathology*; D002450:Cell Communication; D005110:Extracellular Space / Q000378:metabolism; D006801:Humans; D018384:Oxidative Stress; D015398:Signal Transduction; D020521:Stroke / Q000378:metabolism / Q000503:physiopathology*