title: The complement cascade: new avenues in stroke therapy.
abstract: 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.
authors: Department of Neurological Surgery, Columbia University, New York, NY 10011, USA. rjk2103@columbia.edu
authors: Ricardo J
authors: RJ
authors: Komotar
authors: Robert M
authors: RM
authors: Starke
authors: Eric J
authors: EJ
authors: Arias
authors: Matthew C
authors: MC
authors: Garrett
authors: Marc L
authors: ML
authors: Otten
authors: Maxwell B
authors: MB
authors: Merkow
authors: Benjamin
authors: B
authors: Hassid
authors: J
authors: J
authors: Mocco
authors: Michael E
authors: ME
authors: Sughrue
authors: Grace H
authors: GH
authors: Kim
authors: William J
authors: WJ
authors: Mack
authors: Andrew F
authors: AF
authors: Ducruet
authors: E Sander
authors: ES
authors: Connolly
mesh_terms: 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
chemical_list: D051056:Complement Inactivating Agents