The role of complement in the pathogenesis of renal ischemia-reperfusion injury and fibrosisReport as inadecuate




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Fibrogenesis and Tissue Repair

, 7:16

Renal Disease

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.

AbbreviationsaHUSAtypical hemolytic uremic syndrome

AMRAntibody-mediated rejection

C1-INHC1 inhibitor

C5aRC5a receptors

CR1Complement receptor 1

DAMPDanger Associated Molecular Pattern

DGFDelayed graft function

DSADonor specific antibodies

EndMTEndothelial to mesenchymal transition

FDAFood and drug administration

IRIIschemia-reperfusion injury

MACMembrane attack complex

MASPMBL-associated proteins

MBLMannose-binding lectin

PGDPrimary graft dysfunction

PMNsPolymorphonuclear neutrophils

ROSReactive oxygen species.

Electronic supplementary materialThe online version of this article doi:10.1186-1755-1536-7-16 contains supplementary material, which is available to authorized users.

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Author: Juan S Danobeitia - Arjang Djamali - Luis A Fernandez

Source: https://link.springer.com/



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