The DOI matches its Crossref record; 208 of the 208 references it cites were found in a registry or an index.
Inflammogenesis of Secondary Spinal Cord Injury
Open accessAbstract
Spinal cord injury (SCI) and spinal infarction lead to neurological complications and eventually to paraplegia or quadriplegia. These extremely debilitating conditions are major contributors to morbidity. Our understanding of SCI has certainly increased during the last decade, but remains far from clear. SCI consists of two defined phases: the initial impact causes primary injury, which is followed by a prolonged secondary injury consisting of evolving sub-phases that may last for years. The underlying pathophysiological mechanisms driving this condition are complex. Derangement of the vasculature is a notable feature of the pathology of SCI. In particular, an important component of SCI is the ischemia-reperfusion injury (IRI) that leads to endothelial dysfunction and changes in vascular permeability. Indeed, together with endothelial cell damage and failure in homeostasis, ischemia reperfusion injury triggers full-blown inflammatory cascades arising from activation of residential innate immune cells (microglia and astrocytes) and infiltrating leukocytes (neutrophils and macrophages). These inflammatory cells release neurotoxins (proinflammatory cytokines and chemokines, free radicals, excitotoxic amino acids, nitric oxide (NO)), all of which partake in axonal and neuronal deficit. Therefore, our review considers the recent advances in SCI mechanisms, whereby it becomes clear that SCI is a heterogeneous condition. Hence, this leads towards evidence of a restorative approach based on monotherapy with multiple targets or combinatorial treatment. Moreover, from evaluation of the existing literature, it appears that there is an urgent requirement for multi-centered, randomized trials for a large patient population. These clinical studies would offer an opportunity in stratifying SCI patients at high risk and selecting appropriate, optimal therapeutic regimens for personalized medicine.
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Cites
Nitric oxide: physiology, pathophysiology, and pharmacology.
Moncada, S., Palmer, R. M., & Higgs, E. A. (1991) · Pharmacological Reviews · doi:10.1016/s0031-6997(25)06663-3 · Cited by 15,525
The chemokine system in diverse forms of macrophage activation and polarization
MANTOVANI, A., SICA, A., SOZZANI, S., ALLAVENA, P., VECCHI, A., & LOCATI, M. (2004) · Trends in Immunology · doi:10.1016/j.it.2004.09.015 · Cited by 6,534
Ayala, A., Muñoz, M. F., & Argüelles, S. (2014) · Oxidative Medicine and Cellular Longevity · doi:10.1155/2014/360438 · Cited by 6,349
Neutrophil recruitment and function in health and inflammation
Kolaczkowska, E., & Kubes, P. (2013) · Nature Reviews Immunology · doi:10.1038/nri3399 · Cited by 5,472
Macrophage biology in development, homeostasis and disease
Wynn, T. A., Chawla, A., & Pollard, J. W. (2013) · Nature · doi:10.1038/nature12034 · Cited by 4,684 · cited 2×
“Particular attention is being paid in relation to the ratio of pro-inflammatory macrophages (cytokines: IL-1β, IL-6, IL-12, TNF-α) to that of antiinflammatory type (IL-10, IL-13) during ischemia and in resolution of the inflammatory response (Shechter et al., 2009; Wynn et al., 2013; Brown et al., 2014; Zhou et al., 2…”
BackgroundROS as signalling molecules: Mechanisms that generate specificity in ROS homeostasis
D'Autréaux, B., & Toledano, M. B. (2007) · Nature Reviews Molecular Cell Biology · doi:10.1038/nrm2256 · Cited by 3,642
Cellular Scaling Rules for the Brains of Marsupials: Not as “Primitive” as Expected
Dos Santos, S. E., Porfirio, J., da Cunha, F. B., Manger, P. R., Tavares, W., Pessoa, L., Raghanti, M. A., Sherwood, C. C., & Herculano-Houzel, S. (2017) · Brain, Behavior and Evolution · doi:10.1159/000452856 · Cited by 2,642
Mortality over a Period of 10 Years in Patients with Peripheral Arterial Disease
Criqui, M. H., Langer, R. D., Fronek, A., Feigelson, H. S., Klauber, M. R., McCann, T. J., & Browner, D. (1992) · New England Journal of Medicine · doi:10.1056/nejm199202063260605 · Cited by 2,579
Azevedo, F. A. C., Carvalho, L. R. B., Grinberg, L. T., Farfel, J. M., Ferretti, R. E. L., Leite, R. E. P., Filho, W. J., Lent, R., & Herculano‐Houzel, S. (2009) · Journal of Comparative Neurology · doi:10.1002/cne.21974 · Cited by 2,337
Correction of the Anemia of End-Stage Renal Disease with Recombinant Human Erythropoietin
Eschbach, J. W., Egrie, J. C., Downing, M. R., Browne, J. K., & Adamson, J. W. (1987) · New England Journal of Medicine · doi:10.1056/nejm198701083160203 · Cited by 2,005
Cited by
Spinal cord injury: molecular mechanisms and therapeutic interventions
Hu, X., Xu, W., Ren, Y., Wang, Z., He, X., Huang, R., Ma, B., Zhao, J., Zhu, R., & Cheng, L. (2023) · Signal Transduction and Targeted Therapy · doi:10.1038/s41392-023-01477-6 · Cited by 770
Guo, S., Perets, N., Betzer, O., Ben-Shaul, S., Sheinin, A., Michaelevski, I., Popovtzer, R., Offen, D., & Levenberg, S. (2019) · ACS Nano · doi:10.1021/acsnano.9b01892 · Cited by 424
Kobashi, S., Terashima, T., Katagi, M., Nakae, Y., Okano, J., Suzuki, Y., Urushitani, M., & Kojima, H. (2020) · Molecular Therapy · doi:10.1016/j.ymthe.2019.09.004 · Cited by 186
Biomarkers in Spinal Cord Injury: Prognostic Insights and Future Potentials
Albayar, A. A., Roche, A., Swiatkowski, P., Antar, S., Ouda, N., Emara, E., Smith, D. H., Ozturk, A. K., & Awad, B. I. (2019) · Frontiers in Neurology · doi:10.3389/fneur.2019.00027 · Cited by 108
Xia, Y., Zhu, J., Yang, R., Wang, H., Li, Y., & Fu, C. (2023) · Frontiers in Immunology · doi:10.3389/fimmu.2023.1141601 · Cited by 87
Metadata
- Authors
- Anwar, M. A., Al Shehabi, T. S., & Eid, A. H.
- Venue
- Frontiers in Cellular Neuroscience
- Publisher
- Frontiers Media SA
- Published
- 2016-04-13
- Volume
- 10
- Pages
- 98-98
- ISSN
- 1662-5102 (ISSN-L)
- OpenAlex
- W2337694833
- Cited by
- 440
- References
- 208
- FWCI
- 28.40
- Type
- journal article
- Language
- en
- Open access
- gold
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