New insights in the mechanisms of impaired redox signaling and its interplay with inflammation and immunity in multiple sclerosis

Title:

New insights in the mechanisms of impaired redox signaling and its interplay with inflammation and immunity in multiple sclerosis

Creator:

Michaličková, Danica, Šíma, Martin, and Slanař, Ondřej

Identifier:

https://cdk.lib.cas.cz/client/handle/uuid:13304b8d-efe8-4489-bad5-7327313270a8
uuid:13304b8d-efe8-4489-bad5-7327313270a8
doi:10.33549/physiolres.934276

Subject:

inflammation, iron metabolism, oxidative stress, immunity, autoimmune diseases, antioxidants, and mitochondrial dysfunction

Type:

model:article and TEXT

Format:

počítač and online zdroj

Description:

Multiple sclerosis (MS) is an autoimmune neurological disease characterized by chronic inflammation of the central nervous system (CNS), leading to demyelination and axonal damage and resulting in a range of physical, mental or even psychiatric symptoms. Key role of oxidative stress (OS) in the pathogenesis of MS has been suggested, as indicated by the biochemical analysis of cerebrospinal fluid and blood samples, tissue homogenates, and animal models of multiple sclerosis. OS causes demyelination and neurodegeneration directly, by oxidation of lipids, proteins and DNA but also indirectly, by inducing a dysregulation of the immunity and favoring the state of proinflammatory response. In this review, we discuss the interrelated mechanisms of the impaired redox signaling, of which the most important are inflammation-induced production of free radicals by activated immune cells and growth factors, release of iron from myelin sheath during demyelination and mitochondrial dysfunction and consequent energy failure and impaired oxidative phosphorylation. Review also provides an overview of the interplay between inflammation, immunity and OS in MS. Finally, this review also points out new potential targets in MS regarding attenuation of OS and inflammatory response in MS.

Language:

English

Rights:

http://creativecommons.org/publicdomain/mark/1.0/
policy:public

Coverage:

1-19

Source:

Physiological research | 2020 Volume:69 | Number:1

Harvested from:

CDK

Metadata only:

false