Targeting foam cell formation to improve recovery from ischemic stroke
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Affiliation
Department of Immunobiology, University of ArizonaDepartment of Pediatrics, University of Arizona
Departments of Neurology, Neurosurgery, Psychology, Arizona Center on Aging, BIO5 Institute, University of Arizona
Issue Date
2023-06-01
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Academic Press Inc.Citation
Zbesko, Jacob C., et al. "Targeting foam cell formation to improve recovery from ischemic stroke." Neurobiology of Disease 181 (2023): 106130.Journal
Neurobiology of DiseaseRights
© 2023 The Authors. Published by Elsevier Inc. This is an open access article under the CC BY-NC-ND license (https://creativecommons.org/licenses/by-nc-nd/4.0/).Collection Information
This item from the UA Faculty Publications collection is made available by the University of Arizona with support from the University of Arizona Libraries. If you have questions, please contact us at repository@u.library.arizona.edu.Abstract
Inflammation is a crucial part of the healing process after an ischemic stroke and is required to restore tissue homeostasis. However, the inflammatory response to stroke also worsens neurodegeneration and creates a tissue environment that is unfavorable to regeneration for several months, thereby postponing recovery. In animal models, inflammation can also contribute to the development of delayed cognitive deficits. Myeloid cells that take on a foamy appearance are one of the most prominent immune cell types within chronic stroke infarcts. Emerging evidence indicates that they form as a result of mechanisms of myelin lipid clearance becoming overwhelmed, and that they are a key driver of the chronic inflammatory response to stroke. Therefore, targeting lipid accumulation in foam cells may be a promising strategy for improving recovery. The aim of this review is to provide an overview of current knowledge regarding inflammation and foam cell formation in the brain in the weeks and months following ischemic stroke and identify targets that may be amenable to therapeutic intervention. © 2023 The AuthorsNote
Open access articleISSN
0969-9961PubMed ID
37068641Version
Final Published Versionae974a485f413a2113503eed53cd6c53
10.1016/j.nbd.2023.106130
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Except where otherwise noted, this item's license is described as © 2023 The Authors. Published by Elsevier Inc. This is an open access article under the CC BY-NC-ND license (https://creativecommons.org/licenses/by-nc-nd/4.0/).