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Published in: Fibrogenesis & Tissue Repair 1/2014

Open Access 01-12-2014 | Review

The role of complement in the pathogenesis of renal ischemia-reperfusion injury and fibrosis

Authors: Juan S Danobeitia, Arjang Djamali, Luis A Fernandez

Published in: Fibrogenesis & Tissue Repair | Issue 1/2014

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Abstract

The complement system is a major component of innate immunity and has been commonly identified as a central element in host defense, clearance of immune complexes, and tissue homeostasis. After ischemia-reperfusion injury (IRI), the complement system is activated by endogenous ligands that trigger proteolytic cleavage of complement components via the classical, lectin and/or alternative pathway. The result is the formation of terminal complement components C3a, C5a, and the membrane attack complex (C5b-9 or MAC), all of which play pivotal roles in the amplification of the inflammatory response, chemotaxis, neutrophil/monocyte recruitment and activation, and direct tubular cell injury. However, recent evidence suggests that complement activity transcends innate host defense and there is increasing data suggesting complement as a regulator in processes such as allo-immunity, stem cell differentiation, tissue repair, and progression to fibrosis. In this review, we discuss recent advances addressing the role of complement as a regulator of IRI and renal fibrosis after organ donation for transplantation. We will also briefly discuss currently approved therapies that target complement activity in kidney ischemia-reperfusion and transplantation.
Appendix
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Metadata
Title
The role of complement in the pathogenesis of renal ischemia-reperfusion injury and fibrosis
Authors
Juan S Danobeitia
Arjang Djamali
Luis A Fernandez
Publication date
01-12-2014
Publisher
BioMed Central
Published in
Fibrogenesis & Tissue Repair / Issue 1/2014
Electronic ISSN: 1755-1536
DOI
https://doi.org/10.1186/1755-1536-7-16

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