Targeting Microvasculature for Neuroprotection after SCI
Identifieur interne : 000B79 ( Pmc/Curation ); précédent : 000B78; suivant : 000B80Targeting 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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Fassbender</name><affiliation wicri:level="2"><nlm:aff id="Aff1">Kentucky Spinal Cord Injury Research Center, School of Medicine, University of Louisville, Louisville, KY 40292 USA</nlm:aff><country xml:lang="fr">États-Unis</country><placeName><region type="state">Kentucky</region></placeName><wicri:cityArea>Kentucky Spinal Cord Injury Research Center, School of Medicine, University of Louisville, Louisville</wicri:cityArea></affiliation><affiliation wicri:level="2"><nlm:aff id="Aff2">M.D./Ph.D. Program, Louisville, KY 40292 USA</nlm:aff><country xml:lang="fr">États-Unis</country><placeName><region type="state">Kentucky</region></placeName><wicri:cityArea>M.D./Ph.D. Program, Louisville</wicri:cityArea></affiliation><affiliation wicri:level="2"><nlm:aff id="Aff4">Department of Anatomical Sciences and Neurobiology, School of Medicine, University of Louisville, Louisville, KY 40292 USA</nlm:aff><country xml:lang="fr">États-Unis</country><placeName><region type="state">Kentucky</region></placeName><wicri:cityArea>Department of Anatomical Sciences and Neurobiology, School of Medicine, University of Louisville, Louisville</wicri:cityArea></affiliation></author><author><name sortKey="Whittemore, Scott R" sort="Whittemore, Scott R" uniqKey="Whittemore S" first="Scott R." last="Whittemore">Scott R. 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Whittemore</name><affiliation wicri:level="2"><nlm:aff id="Aff1">Kentucky Spinal Cord Injury Research Center, School of Medicine, University of Louisville, Louisville, KY 40292 USA</nlm:aff><country xml:lang="fr">États-Unis</country><placeName><region type="state">Kentucky</region></placeName><wicri:cityArea>Kentucky Spinal Cord Injury Research Center, School of Medicine, University of Louisville, Louisville</wicri:cityArea></affiliation><affiliation wicri:level="2"><nlm:aff id="Aff3">Department of Neurological Surgery, School of Medicine, University of Louisville, Louisville, KY 40292 USA</nlm:aff><country xml:lang="fr">États-Unis</country><placeName><region type="state">Kentucky</region></placeName><wicri:cityArea>Department of Neurological Surgery, School of Medicine, University of Louisville, Louisville</wicri:cityArea></affiliation><affiliation wicri:level="2"><nlm:aff id="Aff4">Department of Anatomical Sciences and Neurobiology, School of Medicine, University of Louisville, Louisville, KY 40292 USA</nlm:aff><country xml:lang="fr">États-Unis</country><placeName><region type="state">Kentucky</region></placeName><wicri:cityArea>Department of Anatomical Sciences and Neurobiology, School of Medicine, University of Louisville, Louisville</wicri:cityArea></affiliation></author><author><name sortKey="Hagg, Theo" sort="Hagg, Theo" uniqKey="Hagg T" first="Theo" last="Hagg">Theo Hagg</name><affiliation wicri:level="2"><nlm:aff id="Aff1">Kentucky Spinal Cord Injury Research Center, School of Medicine, University of Louisville, Louisville, KY 40292 USA</nlm:aff><country xml:lang="fr">États-Unis</country><placeName><region type="state">Kentucky</region></placeName><wicri:cityArea>Kentucky Spinal Cord Injury Research Center, School of Medicine, University of Louisville, Louisville</wicri:cityArea></affiliation><affiliation wicri:level="2"><nlm:aff id="Aff3">Department of Neurological Surgery, School of Medicine, University of Louisville, Louisville, KY 40292 USA</nlm:aff><country xml:lang="fr">États-Unis</country><placeName><region type="state">Kentucky</region></placeName><wicri:cityArea>Department of Neurological Surgery, School of Medicine, University of Louisville, Louisville</wicri:cityArea></affiliation><affiliation wicri:level="2"><nlm:aff id="Aff5">Department of Pharmacology and Toxicology, School of Medicine, University of Louisville, Louisville, KY 40292 USA</nlm:aff><country xml:lang="fr">États-Unis</country><placeName><region type="state">Kentucky</region></placeName><wicri:cityArea>Department of Pharmacology and Toxicology, School of Medicine, University of Louisville, Louisville</wicri:cityArea></affiliation></author></analytic><series><title level="j">Neurotherapeutics</title><idno type="ISSN">1933-7213</idno><idno type="eISSN">1878-7479</idno><imprint><date when="2011">2011</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><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></front></TEI><pmc article-type="research-article"><pmc-comment>The publisher of this article does not allow downloading of the full text in XML form.</pmc-comment>
<front><journal-meta><journal-id journal-id-type="nlm-ta">Neurotherapeutics</journal-id><journal-title-group><journal-title>Neurotherapeutics</journal-title></journal-title-group><issn pub-type="ppub">1933-7213</issn><issn pub-type="epub">1878-7479</issn><publisher><publisher-name>Springer-Verlag</publisher-name><publisher-loc>New York</publisher-loc></publisher></journal-meta><article-meta><article-id pub-id-type="pmid">21360237</article-id><article-id pub-id-type="pmc">3101824</article-id><article-id pub-id-type="publisher-id">29</article-id><article-id pub-id-type="doi">10.1007/s13311-011-0029-1</article-id><article-categories><subj-group subj-group-type="heading"><subject>Review</subject></subj-group></article-categories><title-group><article-title>Targeting Microvasculature for Neuroprotection after SCI</article-title></title-group><contrib-group><contrib contrib-type="author"><name><surname>Fassbender</surname><given-names>Janelle M.</given-names></name><xref ref-type="aff" rid="Aff1">1</xref><xref ref-type="aff" rid="Aff2">2</xref><xref ref-type="aff" rid="Aff4">4</xref></contrib><contrib contrib-type="author"><name><surname>Whittemore</surname><given-names>Scott R.</given-names></name><xref ref-type="aff" rid="Aff1">1</xref><xref ref-type="aff" rid="Aff3">3</xref><xref ref-type="aff" rid="Aff4">4</xref></contrib><contrib contrib-type="author" corresp="yes"><name><surname>Hagg</surname><given-names>Theo</given-names></name><address><email>theo.hagg@louisville.edu</email></address><xref ref-type="aff" rid="Aff1">1</xref><xref ref-type="aff" rid="Aff3">3</xref><xref ref-type="aff" rid="Aff5">5</xref></contrib><aff id="Aff1"><label>1</label>Kentucky Spinal Cord Injury Research Center, School of Medicine, University of Louisville, Louisville, KY 40292 USA</aff><aff id="Aff2"><label>2</label>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><aff id="Aff5"><label>5</label>Department of Pharmacology and Toxicology, School of Medicine, University of Louisville, Louisville, KY 40292 USA</aff></contrib-group><pub-date pub-type="epub"><day>1</day><month>3</month><year>2011</year></pub-date><pub-date pub-type="ppub"><month>4</month><year>2011</year></pub-date><volume>8</volume><issue>2</issue><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></kwd-group><custom-meta-group><custom-meta><meta-name>issue-copyright-statement</meta-name><meta-value>© The American Society for Experimental NeuroTherapeutics, Inc. 2011</meta-value></custom-meta></custom-meta-group></article-meta></front></pmc></record>Pour manipuler ce document sous Unix (Dilib)
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