title: Cellular mechanisms of neurovascular damage and repair after stroke.
abstract: The biological processes underlying stroke are complex, and patients have a narrow repertoire of therapeutic opportunities. After the National Institutes of Health (NIH) convened the Stroke Progress Review Group in 2001, stroke research shifted from having a purely neurocentric focus to adopting a more integrated view wherein dynamic interactions between all cell types contribute to function and dysfunction in the brain. This so-called "neurovascular unit" provides a conceptual framework that emphasizes cell-cell interactions between neuronal, glial, and vascular elements. Under normal conditions, signaling within the neurovascular unit helps maintain homeostasis. After stroke, cell-cell signaling is disturbed, leading to pathophysiology. More recently, emerging data now suggest that these cell-cell signaling mechanisms may also mediate parallel processes of neurovascular remodeling during stroke recovery. Because plasticity is a signature feature of the young and developing brain, these concepts may have special relevance to how the pediatric brain responds after stroke.
authors.affiliation: The Neuroprotection Research Laboratory, Departments of Radiology and Neurology, Massachusetts General Hospital, and Harvard Medical School, Boston, Massachusetts, USA. karai@partners.org
authors.forename: Ken
authors.initials: K
authors.lastname: Arai
authors.forename: Josephine
authors.initials: J
authors.lastname: Lok
authors.forename: Shuzhen
authors.initials: S
authors.lastname: Guo
authors.forename: Kazuhide
authors.initials: K
authors.lastname: Hayakawa
authors.forename: Changhong
authors.initials: C
authors.lastname: Xing
authors.forename: Eng H
authors.initials: EH
authors.lastname: Lo
mesh_terms: D000818:Animals; D001812:Blood-Brain Barrier / Q000503:physiopathology; D001921:Brain / Q000196:embryology / Q000254:growth & development / Q000473:pathology*; D002450:Cell Communication / Q000502:physiology; D006801:Humans; D009389:Neovascularization, Pathologic / Q000209:etiology*; D055495:Neurogenesis / Q000502:physiology*; D009474:Neurons / Q000502:physiology*; D020521:Stroke / Q000150:complications* / Q000473:pathology*