Complement mediators in ischemia-reperfusion injury

Arumugam, Thiruma V., Magnus, Tim, Woodruff, Trent M., Proctor, Lavinia M., Shiels, Ian A., Taylor, Stephen M., A. H. Wu and J. Delanghe (2006) Complement mediators in ischemia-reperfusion injury. Clinica Chimica Acta, 374 1-2: 33-45. doi:10.1016/j.cca.2006.06.010


Author Arumugam, Thiruma V.
Magnus, Tim
Woodruff, Trent M.
Proctor, Lavinia M.
Shiels, Ian A.
Taylor, Stephen M.
A. H. Wu
J. Delanghe
Title Complement mediators in ischemia-reperfusion injury
Journal name Clinica Chimica Acta   Check publisher's open access policy
ISSN 0009-8981
1873-3492
Publication date 2006-12-01
Sub-type Article (original research)
DOI 10.1016/j.cca.2006.06.010
Volume 374
Issue 1-2
Start page 33
End page 45
Total pages 13
Place of publication Amsterdam
Publisher Elsevier Science Bv
Language eng
Subject C1
06 Biological Sciences
Formatted abstract
Background
Ischemia–reperfusion (I/R) injury occurs when a tissue is temporarily deprived of blood supply and the return of the blood supply triggers an intense inflammatory response. Pathologically, increased complement activity can cause substantial damage to blood vessels, tissues and also facilitate leukocyte activation and recruitment following I/R injury. Herein, previously published studies are reported and critically reviewed.

Methods

Medline and the World Wide Web were searched and the relevant literature was classified under the following categories: (1) Complement pathways; (2) The complement system and the inflammatory response; (3) Complement in ischemia–reperfusion injuries; and (4) Therapeutic approaches against complement in I/R injuries.

Results and conclusions

I/R injury is a common clinical event with the potential to seriously affect, and sometimes kill, the patient and is a potent inducer of complement activation that results in the production of a number of inflammatory mediators. Complement activation leads to the release of biologically active potent inflammatory complement substances including the anaphylatoxins (C3a and C5a) and the cytolytic terminal membrane attack complement complex C5b-9 (MAC). The use of specific complement inhibitors to block complement activation at various levels of the cascade has been shown to prevent or reduce local tissue injury after I/R. Several agents that inhibit all or part of the complement system, such as soluble complement receptor type 1 (sCR1), C1 inhibitor (C1-INH), C5a monoclonal antibodies, a C5a receptor antagonist and soluble CD59 (sCD59) have been shown to reduce I/R injury of various organs. The novel inhibitors of complement products may eventually find wide clinical application because there are no effective drug therapies currently available to treat I/R injuries.
Keyword Ischemia-reperfusion
Complement
C5a
Membrane Attack Complex
Inflammation
Medical Laboratory Technology
C5a Receptor Antagonist
Acute Myocardial-infarction
Remote Organ Injury
Respiratory-distress-syndrome
Inflammatory-bowel-disease
Human Endothelial-cells
Mannose-binding Lectin
C1 Esterase Inhibitor
Lower Torso Ischemia
Q-Index Code C1
Additional Notes This document is a journal review.

 
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Created: Wed, 15 Aug 2007, 19:43:29 EST