The complement cascade: new avenues in stroke therapy.
Recent evidence has shown that after the initial occlusion, a large portion of stroke patients achieve some degree of reperfusion either through collateral circulation or clot dissolution. However, it appears that this reperfusion may lead to increased inflammation-induced damage. Even though the exact mechanism of this secondary injury is unclear, several experimental studies have indicated an intimate connection between complement and this secondary form of damage. We review the available literature and attempt to identify promising clinical therapeutic targets.
Komotar
Ricardo J
RJ
Department of Neurological Surgery, Columbia University, New York, NY 10011, USA. rjk2103@columbia.edu
Starke
Robert M
RM
Arias
Eric J
EJ
Garrett
Matthew C
MC
Otten
Marc L
ML
Merkow
Maxwell B
MB
Hassid
Benjamin
B
Mocco
J
J
Sughrue
Michael E
ME
Kim
Grace H
GH
Mack
William J
WJ
Ducruet
Andrew F
AF
Connolly
E Sander
ES
D000818:Animals; D001921:Brain / Q000503:physiopathology; D003167:Complement Activation / Q000187:drug effects* / Q000502:physiology; D051056:Complement Inactivating Agents / Q000627:therapeutic use*; D004195:Disease Models, Animal; D006801:Humans; D008954:Models, Biological; D055495:Neurogenesis / Q000187:drug effects; D015427:Reperfusion Injury / Q000188:drug therapy* / Q000503:physiopathology; D020521:Stroke / Q000150:complications / Q000188:drug therapy* / Q000503:physiopathology
D051056:Complement Inactivating Agents