Open AccessSenicapoc: Repurposing a Drug to Target Microglia KCa3.1 in Stroke
Author(s) -
Roland G. W. Staal,
Jonathan R. Weinstein,
Megan Nattini,
Manuel Cajina,
Gamini Chandresana,
Thomas Möller
Publication year - 2017
Publication title -
neurochemical research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.102
H-Index - 116
eISSN - 1573-6903
pISSN - 0364-3190
DOI - 10.1007/s11064-017-2223-y
Subject(s) - microglia , stroke (engine) , neuroinflammation , inflammation , medicine , neuroprotection , neuroscience , pathophysiology , neurology , ischemia , immune system , pharmacology , immunology , biology , mechanical engineering , engineering
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 K Ca 3.1 is expressed selectively in the injured CNS by microglia. K Ca 3.1 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 K Ca 3.1 inhibitor, to intervene in the inflammation cascade that follows ischemia/reperfusion.