The DOI matches its Crossref record; 10 of the 10 references it cites were found in a registry or an index.
Degenerative and regenerative mechanisms governing spinal cord injury
Open accessAbstract
Spinal cord injury (SCI) is a major cause of disability, and at present, there is no universally accepted treatment. The functional decline following SCI is contributed to both direct mechanical injury and secondary pathophysiological mechanisms that are induced by the initial trauma. These mechanisms initially involve widespread haemorrhage at the site of injury and necrosis of central nervous system (CNS) cellular components. At later stages of injury, the cord is observed to display reactive gliosis. The actions of astrocytes as well as numerous other cells in this response create an environment that is highly nonpermissive to axonal regrowth. Also manifesting important effects is the immune system. The early recruitment of neutrophils and at later stages, macrophages to the site of insult cause exacerbation of injury. However, at more chronic stages, macrophages and recruited T helper cells may potentially be helpful by providing trophic support for neuronal and non-neuronal components of the injured CNS. Within this sea of injurious mechanisms, the oligodendrocytes appear to be highly vulnerable. At chronic stages of SCI, a large number of oligodendrocytes undergo apoptosis at sites that are distant to the vicinity of primary injury. This leads to denudement of axons and deterioration of their conductive abilities, which adds significantly to functional decline. By indulging into the molecular mechanisms that cause oligodendrocyte apoptosis and identifying potential targets for therapeutic intervention, the prevention of this apoptotic wave will be of tremendous value to individuals living with SCI.
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Citations
Cites
Chondroitinase ABC promotes functional recovery after spinal cord injury
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The p75 receptor acts as a displacement factor that releases Rho from Rho-GDI
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Cited by
Donnelly, D. J., & Popovich, P. G. (2008) · Experimental Neurology · doi:10.1016/j.expneurol.2007.06.009 · Cited by 995
Bringmann, A., Iandiev, I., Pannicke, T., Wurm, A., Hollborn, M., Wiedemann, P., Osborne, N. N., & Reichenbach, A. (2009) · Progress in Retinal and Eye Research · doi:10.1016/j.preteyeres.2009.07.001 · Cited by 761
Reactive Astrogliosis after Spinal Cord Injury—Beneficial and Detrimental Effects
Karimi-Abdolrezaee, S., & Billakanti, R. (2012) · Molecular Neurobiology · doi:10.1007/s12035-012-8287-4 · Cited by 331
Duan, H., Ge, W., Zhang, A., Xi, Y., Chen, Z., Luo, D., Cheng, Y., Fan, K. S., Horvath, S., Sofroniew, M. V., et al. (2015) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.1510176112 · Cited by 115
Kibaly, C., Patte‐Mensah, C., & Mensah‐Nyagan, A. G. (2005) · Journal of Neurochemistry · doi:10.1111/j.1471-4159.2005.03113.x · Cited by 66
Metadata
- Authors
- Profyris, C., Cheema, S. S., Zang, D., Azari, M. F., Boyle, K., & Petratos, S.
- Venue
- Neurobiology of Disease
- Publisher
- Elsevier BV
- Published
- 2004-04
- Volume
- 15
- Issue
- 3
- Pages
- 415-436
- ISSN
- 0969-9961 (ISSN-L)
- OpenAlex
- W1977494370
- Cited by
- 458
- References
- 10
- FWCI
- 12.26
- Type
- journal article
- Language
- en
- Open access
- green
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Bibliographic data: Semantic Scholar, OpenAlex, Crossref.
Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.
