The role of the complement system in ischemia-reperfusion injury.
Ischemia-reperfusion (I/R) injury is a common clinical event with the potential to seriously affect, and sometimes kill, the patient. Interruption of blood supply causes ischemia, which rapidly damages metabolically active tissues. Paradoxically, restoration of blood flow to the ischemic tissues initiates a cascade of pathology that leads to additional cell or tissue injury. I/R is a potent inducer of complement activation that results in the production of a number of inflammatory mediators. The use of specific inhibitors to block complement activation has been shown to prevent local tissue injury after I/R. Clinical and experimental studies in gut, kidney, limb, and liver have shown that I/R results in local activation of the complement system and leads to the production of the complement factors C3a, C5a, and the membrane attack complex. The novel inhibitors of complement products may find wide clinical application because there are no effective drug therapies currently available to treat I/R injuries.
Arumugam
Thiruma V
TV
Department of Molecular & Cellular Physiology, Louisiana State University Health Sciences Center, Shreveport, Louisiana 71130-3932, USA.
Shiels
Ian A
IA
Woodruff
Trent M
TM
Granger
D Neil
DN
Taylor
Stephen M
SM
D000818:Animals; D002462:Cell Membrane / Q000378:metabolism; D003182:Complement C5 / Q000378:metabolism; D015936:Complement C5a / Q000378:metabolism; D003165:Complement System Proteins / Q000502:physiology*; D006801:Humans; D007249:Inflammation; D007422:Intestines / Q000473:pathology; D007668:Kidney / Q000473:pathology; D008099:Liver / Q000473:pathology; D018482:Muscle, Skeletal / Q000473:pathology; D015427:Reperfusion Injury / Q000628:therapy*
D003182:Complement C5; D015936:Complement C5a; D003165:Complement System Proteins