The DOI matches its Crossref record; 196 of the 196 references it cites were found in a registry or an index.
Post-stroke inflammation—target or tool for therapy?
Open accessAbstract
Inflammation is currently considered a prime target for the development of new stroke therapies. In the acute phase of ischemic stroke, microglia are activated and then circulating immune cells invade the peri-infarct and infarct core. Resident and infiltrating cells together orchestrate the post-stroke inflammatory response, communicating with each other and the ischemic neurons, through soluble and membrane-bound signaling molecules, including cytokines. Inflammation can be both detrimental and beneficial at particular stages after a stroke. While it can contribute to expansion of the infarct, it is also responsible for infarct resolution, and influences remodeling and repair. Several pre-clinical and clinical proof-of-concept studies have suggested the effectiveness of pharmacological interventions that target inflammation post-stroke. Experimental evidence shows that targeting certain inflammatory cytokines, such as tumor necrosis factor, interleukin (IL)-1, IL-6, and IL-10, holds promise. However, as these cytokines possess non-redundant protective and immunoregulatory functions, their neutralization or augmentation carries a risk of unwanted side effects, and clinical translation is, therefore, challenging. This review summarizes the cell biology of the post-stroke inflammatory response and discusses pharmacological interventions targeting inflammation in the acute phase after a stroke that may be used alone or in combination with recanalization therapies. Development of next-generation immune therapies should ideally aim at selectively neutralizing pathogenic immune signaling, enhancing tissue preservation, promoting neurological recovery and leaving normal function intact.
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Cites
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Cited by
Neuroinflammation: friend and foe for ischemic stroke
Jayaraj, R. L., Azimullah, S., Beiram, R., Jalal, F. Y., & Rosenberg, G. A. (2019) · Journal of Neuroinflammation · doi:10.1186/s12974-019-1516-2 · Cited by 1,428
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Glial Cells: Role of the Immune Response in Ischemic Stroke
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Interleukins and Ischemic Stroke
Zhu, H., Hu, S., Li, Y., Sun, Y., Xiong, X., Hu, X., Chen, J., & Qiu, S. (2022) · Frontiers in Immunology · doi:10.3389/fimmu.2022.828447 · Cited by 363
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
Metadata
- Authors
- Lambertsen, K. L., Finsen, B., & Clausen, B. H.
- Venue
- Acta Neuropathologica
- Published
- 2018-11-27
- Volume
- 137
- Issue
- 5
- Pages
- 693-714
- ISSN
- 0001-6322 (ISSN-L)
- 1432-0533
- OpenAlex
- W2900430109
- Cited by
- 465
- References
- 196
- FWCI
- 13.15
- Type
- journal article
- Language
- en
- Open access
- hybrid
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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
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