Dysfunctional K+ homeostasis as a driver for brain inflammation

[thumbnail of Open Access]
Preview
Text (Open Access) - Published Version
· Available under License Creative Commons Attribution.
· Please see our End User Agreement before downloading.
| Preview
Available under license: Creative Commons Attribution

Please see our End User Agreement.

It is advisable to refer to the publisher's version if you intend to cite from this work. See Guidance on citing.

Add to AnyAdd to TwitterAdd to FacebookAdd to LinkedinAdd to PinterestAdd to Email

Ozsoy, N. orcid id iconORCID: https://orcid.org/0000-0001-6269-9484 and Dallas, M. L. orcid id iconORCID: https://orcid.org/0000-0002-5190-0522 (2024) Dysfunctional K+ homeostasis as a driver for brain inflammation. Encyclopedia, 4 (4). pp. 1681-1699. ISSN 2673-8392 doi: 10.3390/encyclopedia4040110

Abstract/Summary

The central nervous system (CNS) relies on precise regulation of potassium ion (K+) concentrations to maintain physiology. This regulation involves complex cellular and molecular mechanisms that work in concert to regulate both intracellular and extracellular K+ levels. Inflammation, a key physiological response, encompasses a series of cell-specific events leading to inflammasome activation. Perturbations in K+-sensitive processes can result in either chronic or uncontrolled inflammation, highlighting the intricate relationship between K+ homeostasis and inflammatory signalling. This review explores molecular targets that influence K+ homeostasis and have been implicated in inflammatory cascades, offering potential therapeutic avenues for managing inflammation. We examine both cell-specific and common molecular targets across different cell types, providing a comprehensive overview of the interplay between K+ regulation and inflammation in the CNS. By elucidating these mechanisms, we identify leads for drug discovery programmes aimed at modulating inflammatory responses. Additionally, we highlight potential consequences of targeting individual molecular entities for therapeutic purposes, emphasizing the need for a nuanced approach in developing anti-inflammatory strategies. This review considers current knowledge on K+-sensitive inflammatory processes within the CNS, offering critical insights into the molecular underpinnings of inflammation and potential therapeutic interventions. Our findings underscore the importance of considering K+ homeostasis in the development of targeted therapies for inflammatory conditions within the CNS.

Altmetric Badge

Item Type Article
URI https://reading-clone.eprints-hosting.org/id/eprint/119687
Identification Number/DOI 10.3390/encyclopedia4040110
Refereed Yes
Divisions Life Sciences > School of Chemistry, Food and Pharmacy > School of Pharmacy
Publisher MDPI
Download/View statistics View download statistics for this item

Downloads

Downloads per month over past year

University Staff: Request a correction | Centaur Editors: Update this record

Search Google Scholar