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Vascular Mechanisms in Spinal Cord Injury

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Book cover Vascular Mechanisms in CNS Trauma

Part of the book series: Springer Series in Translational Stroke Research ((SSTSR,volume 5))

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Abstract

This review provides an introduction to the field of vascular dysfunction as a cause of secondary degeneration following traumatic spinal cord injury. Major breakthroughs have been made by using endothelial cell-selective treatments to show that endothelial cell survival and function is key to protecting the spinal cord tissue. Other vascular treatment strategies involve the reduction of detrimental leakage and improving microvascular perfusion and function. The toxicity of the acutely developing hemorrhage most likely is a major problem but has not been solved so far. The role of angiogenesis in spinal cord injury remains unclear. The advances made between late 2011 and the end of 2012 in understanding molecular mechanisms and opportunities for therapeutic intervention receive particular attention. Lastly, future directions are discussed, including the need for microvascular diagnostic tools and challenges of clinical translation.

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Abbreviations

BSCB:

Blood–spinal cord-barrier

CHOP:

CCAAT enhancer binding protein (C/EBP) homologous protein

FGF2:

Fibroblast growth factor 2 (basic)

JNK:

c-Jun N-terminal kinase

PDGF:

Platelet-derived growth factor

Sur1:

Sulfonylurea receptor 1

TRPM4:

Transient receptor potential cation channel, subfamily M, member 4

VEGF:

Vascular endothelial growth factor

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Acknowledgements

Justin Geralds is thanked for his contribution to Fig. 9.3. Supported by NIH grant NS045734 and the Commonwealth of Kentucky Challenge for Excellence.

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Hagg, T. (2014). Vascular Mechanisms in Spinal Cord Injury. In: Lo, E., Lok, J., Ning, M., Whalen, M. (eds) Vascular Mechanisms in CNS Trauma. Springer Series in Translational Stroke Research, vol 5. Springer, New York, NY. https://doi.org/10.1007/978-1-4614-8690-9_9

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