title: Targeting microvasculature for neuroprotection after SCI.
abstract: Spinal cord injury (SCI) is characterized by secondary degeneration, which leads to tissue loss at the epicenter and subsequent functional deficits. This review provides insight into the pathophysiology of microvascular dysfunction and endothelial cell loss, which are among the earliest responses during the first postinjury day. The enigmatic role of the angiogenic response in the penumbra around the lost tissue, which occurs during the first 2 weeks, is also discussed. The importance of stabilizing and rescuing the injured vasculature is now well-recognized, and several pharmacological and genetic treatments have emerged in the past few years. We conclude with suggestions for future experimental research, including development of vascular-selective treatments and exploitation of genetic models. In summary, vascular dysfunction following SCI is an important contributor to neurological deficits, as proposed long ago. However, there now appears to be new and potentially powerful opportunities for treating acute SCI by targeting the vascular responses.
authors.affiliation: Kentucky Spinal Cord Injury Research Center, School of Medicine, University of Louisville, Louisville, KY 40292, USA.
authors.forename: Janelle M
authors.initials: JM
authors.lastname: Fassbender
authors.forename: Scott R
authors.initials: SR
authors.lastname: Whittemore
authors.forename: Theo
authors.initials: T
authors.lastname: Hagg
mesh_terms: D000818:Animals; D002560:Cerebrovascular Circulation / Q000187:drug effects / Q000502:physiology; D006801:Humans; D055806:Microvessels / Q000187:drug effects / Q000473:pathology*; D018919:Neovascularization, Physiologic / Q000187:drug effects / Q000502:physiology; D009410:Nerve Degeneration / Q000473:pathology / Q000503:physiopathology; D018696:Neuroprotective Agents / Q000494:pharmacology; D013119:Spinal Cord Injuries / Q000473:pathology* / Q000503:physiopathology
chemical_list: D018696:Neuroprotective Agents