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Updated: Jun 4, 2026

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Targeting microvasculature for neuroprotection after SCI.

Janelle M Fassbender1, Scott R Whittemore, Theo Hagg

  • 1Kentucky Spinal Cord Injury Research Center, School of Medicine, University of Louisville, Louisville, KY 40292, USA.

Neurotherapeutics : the Journal of the American Society for Experimental Neurotherapeutics
|March 2, 2011
PubMed
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Spinal cord injury (SCI) causes early vascular damage, leading to tissue loss and functional deficits. Targeting these vascular responses offers new therapeutic opportunities for acute SCI treatment.

Area of Science:

  • Neuroscience
  • Vascular Biology
  • Regenerative Medicine

Background:

  • Spinal cord injury (SCI) triggers secondary degeneration, resulting in tissue loss and functional deficits.
  • Early responses include microvascular dysfunction and endothelial cell loss within the first day post-injury.

Purpose of the Study:

  • To review the pathophysiology of vascular changes following SCI.
  • To discuss the role of angiogenic responses in the injury penumbra.
  • To highlight the therapeutic potential of targeting vascular responses in acute SCI.

Main Methods:

  • Literature review focusing on pathophysiology of vascular dysfunction after SCI.
  • Analysis of early cellular and molecular responses.
  • Discussion of emerging pharmacological and genetic treatments.

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Last Updated: Jun 4, 2026

Assessment of Vascular Regeneration in the CNS Using the Mouse Retina
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Assessment of Vascular Regeneration in the CNS Using the Mouse Retina

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Mouse Microsurgery Infusion Technique for Targeted Substance Delivery into the CNS via the Internal Carotid Artery
06:41

Mouse Microsurgery Infusion Technique for Targeted Substance Delivery into the CNS via the Internal Carotid Artery

Published on: January 31, 2017

Main Results:

  • Microvascular dysfunction and endothelial cell loss are critical early events in SCI.
  • The angiogenic response in the injury vicinity has a complex, debated role.
  • Stabilizing and rescuing injured vasculature is crucial for mitigating SCI progression.

Conclusions:

  • Vascular dysfunction significantly contributes to neurological deficits after SCI.
  • Emerging treatments targeting vascular responses present promising therapeutic avenues for acute SCI.
  • Future research should focus on vascular-selective treatments and genetic models.