Targeting Microvasculature for Neuroprotection after SCI
Identifieur interne : 004162 ( Ncbi/Merge ); précédent : 004161; suivant : 004163Targeting Microvasculature for Neuroprotection after SCI
Auteurs : Janelle M. Fassbender [États-Unis] ; Scott R. Whittemore [États-Unis] ; Theo Hagg [États-Unis]Source :
- Neurotherapeutics [ 1933-7213 ] ; 2011.
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.
The online version of this article (doi:10.1007/s13311-011-0029-1) contains supplementary material, which is available to authorized users.
Url:
DOI: 10.1007/s13311-011-0029-1
PubMed: 21360237
PubMed Central: 3101824
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<front><div type="abstract" xml:lang="en"><title>Summary</title>
<p>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.</p>
<sec><title>Electronic supplementary material</title>
<p>The online version of this article (doi:10.1007/s13311-011-0029-1) contains supplementary material, which is available to authorized users.</p>
</sec>
</div>
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<title-group><article-title>Targeting Microvasculature for Neuroprotection after SCI</article-title>
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<contrib-group><contrib contrib-type="author"><name><surname>Fassbender</surname>
<given-names>Janelle M.</given-names>
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<xref ref-type="aff" rid="Aff1">1</xref>
<xref ref-type="aff" rid="Aff2">2</xref>
<xref ref-type="aff" rid="Aff4">4</xref>
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<contrib contrib-type="author"><name><surname>Whittemore</surname>
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Kentucky Spinal Cord Injury Research Center, School of Medicine, University of Louisville, Louisville, KY 40292 USA</aff>
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M.D./Ph.D. Program, Louisville, KY 40292 USA</aff>
<aff id="Aff3"><label>3</label>
Department of Neurological Surgery, School of Medicine, University of Louisville, Louisville, KY 40292 USA</aff>
<aff id="Aff4"><label>4</label>
Department of Anatomical Sciences and Neurobiology, School of Medicine, University of Louisville, Louisville, KY 40292 USA</aff>
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Department of Pharmacology and Toxicology, School of Medicine, University of Louisville, Louisville, KY 40292 USA</aff>
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<fpage>240</fpage>
<lpage>251</lpage>
<permissions><copyright-statement>© The American Society for Experimental NeuroTherapeutics, Inc. 2011</copyright-statement>
</permissions>
<abstract id="Abs1"><title>Summary</title>
<p>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.</p>
<sec><title>Electronic supplementary material</title>
<p>The online version of this article (doi:10.1007/s13311-011-0029-1) contains supplementary material, which is available to authorized users.</p>
</sec>
</abstract>
<kwd-group><title>Key Words</title>
<kwd>Spinal cord injury</kwd>
<kwd>therapeutics</kwd>
<kwd>neuroprotection</kwd>
<kwd>vasculature</kwd>
<kwd>inflammation</kwd>
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<custom-meta-group><custom-meta><meta-name>issue-copyright-statement</meta-name>
<meta-value>© The American Society for Experimental NeuroTherapeutics, Inc. 2011</meta-value>
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