Therapeutic Potential of Cytokines in Demyelinating Lesions After Stroke.

Abstract

White matter damage is a component of most human stroke and usually accounts for at least half of the lesion volume. Subcortical white matter stroke (WMS) accounts for 25% of all strokes and causes severe motor and cognitive dysfunction. The adult brain has a very limited ability to repair white matter damage. Pathological analysis shows that demyelination or myelin loss is the main feature of white matter injury and plays an important role in long-term sensorimotor and cognitive dysfunction. This suggests that demyelination is a major therapeutic target for ischemic stroke injury. An acute inflammatory reaction is triggered by brain ischemia, which is accompanied by cytokine production. The production of cytokines is an important factor affecting demyelination and myelin regeneration. Different cytokines have different effects on myelin damage and myelin regeneration. Exploring the role of cytokines in demyelination and remyelination after stroke and the underlying molecular mechanisms of demyelination and myelin regeneration after ischemic injury is very important for the development of rehabilitation treatment strategies. This review focuses on recent findings on the effects of cytokines on myelin damage and remyelination as well as the progress of research on the role of cytokines in ischemic stroke prognosis to provide a new treatment approach for amelioration of white matter damage after stroke.

• Authors: Yi-Sha Guo, Mei Yuan, Yu Han, Xin-Ya Shen, Zhen-Kun Gao, Xia Bi
• Journal: Journal of molecular neuroscience : MN (J Mol Neurosci) Vol. 71 Issue 10 Pg. 2035-2052 (Oct 2021) ISSN: 1559-1166 [Electronic] United States
• PMID: 33970426 (Publication Type: Journal Article, Review)
• Copyright: © 2021. The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature.

Chemical References

• Chemokines
• Interleukins
• Receptors, CXCR

Topics

• Animals
• Chemokines (metabolism, therapeutic use)
• Demyelinating Diseases (drug therapy, etiology, metabolism)
• Humans
• Interleukins (metabolism, therapeutic use)
• Nerve Regeneration
• Receptors, CXCR (metabolism)
• Stroke (complications, drug therapy, metabolism)