Senicapoc: Repurposing a Drug to Target Microglia K^sub Ca^3.1 in Stroke

Stroke is the leading cause of serious long-term disability and the fifth leading cause of death in the United States. Treatment options for stroke are few in number and limited in efficacy. Neuroinflammation mediated by microglia and infiltrating peripheral immune cells is a major component of stro...

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Bibliographic Details
Published in:Neurochemical research 2017-09, Vol.42 (9), p.2639
Main Authors: Staal, Roland G, W, Weinstein, Jonathan R, Nattini, Megan, Cajina, Manuel, Chandresana, Gamini, Möller, Thomas
Format: Article
Language:English
Subjects:
Brain
Brain injury
Calcium
Central nervous system
Head injuries
Immune system
Inflammation
Ischemia
Microglia
Potassium
Reperfusion
Stroke
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Summary:Stroke is the leading cause of serious long-term disability and the fifth leading cause of death in the United States. Treatment options for stroke are few in number and limited in efficacy. Neuroinflammation mediated by microglia and infiltrating peripheral immune cells is a major component of stroke pathophysiology. Interfering with the inflammation cascade after stroke holds the promise to modulate stroke outcome. The calcium activated potassium channel KCa3.1 is expressed selectively in the injured CNS by microglia. KCa3.1 function has been implicated in pro-inflammatory activation of microglia and there is recent literature suggesting that this channel is important in the pathophysiology of ischemia/reperfusion (stroke) related brain injury. Here we describe the potential of repurposing Senicapoc, a KCa3.1 inhibitor, to intervene in the inflammation cascade that follows ischemia/reperfusion.
ISSN:0364-3190
1573-6903
DOI:10.1007/s11064-017-2223-y