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.
Medical Subject Headings
Animals; Brain (physiopathology); Complement Activation (drug effects, physiology); Complement Inactivating Agents (therapeutic use); Disease Models, Animal; Humans; Models, Biological; Neurogenesis (drug effects); Reperfusion Injury (drug therapy, physiopathology); Stroke (complications, drug therapy, physiopathology)
Current vascular pharmacology
Digital Object Identifier (DOI)
Komotar, Ricardo J.; Starke, Robert M.; Arias, Eric J.; Garrett, Matthew C.; Otten, Marc L.; Merkow, Maxwell B.; Hassid, Benjamin; Mocco, J; Sughrue, Michael E.; Kim, Grace H.; Mack, William J.; Ducruet, Andrew F.; and Connolly, E Sander, "The complement cascade: new avenues in stroke therapy" (2009). Translational Neuroscience. 2174.