The DOI matches its Crossref record; 32 of the 32 references it cites were found in a registry or an index.
Neuroinflammation: friend and foe for ischemic stroke
Open accessAbstract
Stroke, the third leading cause of death and disability worldwide, is undergoing a change in perspective with the emergence of new ideas on neurodegeneration. The concept that stroke is a disorder solely of blood vessels has been expanded to include the effects of a detrimental interaction between glia, neurons, vascular cells, and matrix components, which is collectively referred to as the neurovascular unit. Following the acute stroke, the majority of which are ischemic, there is secondary neuroinflammation that both promotes further injury, resulting in cell death, but conversely plays a beneficial role, by promoting recovery. The proinflammatory signals from immune mediators rapidly activate resident cells and influence infiltration of a wide range of inflammatory cells (neutrophils, monocytes/macrophages, different subtypes of T cells, and other inflammatory cells) into the ischemic region exacerbating brain damage. In this review, we discuss how neuroinflammation has both beneficial as well as detrimental roles and recent therapeutic strategies to combat pathological responses. Here, we also focus on time-dependent entry of immune cells to the ischemic area and the impact of other pathological mediators, including oxidative stress, excitotoxicity, matrix metalloproteinases (MMPs), high-mobility group box 1 (HMGB1), arachidonic acid metabolites, mitogen-activated protein kinase (MAPK), and post-translational modifications that could potentially perpetuate ischemic brain damage after the acute injury. Understanding the time-dependent role of inflammatory factors could help in developing new diagnostic, prognostic, and therapeutic neuroprotective strategies for post-stroke inflammation.
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Cited by
Factors influencing the blood-brain barrier permeability
Zhao, Y., Gan, L., Ren, L., Lin, Y., Ma, C., & Lin, X. (2022) · Brain Research · doi:10.1016/j.brainres.2022.147937 · Cited by 291
New insight into neurological degeneration: Inflammatory cytokines and blood–brain barrier
Yang, J., Ran, M., Li, H., Lin, Y., Ma, K., Yang, Y., Fu, X., & Yang, S. (2022) · Frontiers in Molecular Neuroscience · doi:10.3389/fnmol.2022.1013933 · Cited by 279
Fernández-Calle, R., Konings, S. C., Frontiñán-Rubio, J., García-Revilla, J., Camprubí-Ferrer, L., Svensson, M., Martinson, I., Boza-Serrano, A., Venero, J. L., Nielsen, H. M., et al. (2022) · Molecular Neurodegeneration · doi:10.1186/s13024-022-00566-4 · Cited by 278
Werner, Y., Mass, E., Ashok Kumar, P., Ulas, T., Händler, K., Horne, A., Klee, K., Lupp, A., Schütz, D., Saaber, F., et al. (2020) · Nature Neuroscience · doi:10.1038/s41593-020-0585-y · Cited by 208
Mithaiwala, M. N., Santana-Coelho, D., Porter, G. A., & O’Connor, J. C. (2021) · Cells · doi:10.3390/cells10061548 · Cited by 190
Metadata
- Authors
- Jayaraj, R. L., Azimullah, S., Beiram, R., Jalal, F. Y., & Rosenberg, G. A.
- Venue
- Journal of Neuroinflammation
- Published
- 2019-07-10
- Volume
- 16
- Issue
- 1
- Pages
- 142-142
- ISSN
- 1742-2094 (ISSN-L)
- OpenAlex
- W2959218190
- Cited by
- 1,428
- References
- 32
- FWCI
- 51.16
- Type
- journal article
- Language
- en
- Open access
- gold
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