Which pathways trigger the role of complement in ischaemia?reperfusion injury?.pdf (297.65 kB)
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Which pathways trigger the role of complement in ischaemia/reperfusion injury?

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journal contribution
posted on 31.10.2016, 10:28 by C. A. Farrar, E. Asgari, Wilhelm J. Schwaeble, S. H. Sacks
Investigations into the role of complement in ischemia/reperfusion (I/R) injury have identified common effector mechanisms that depend on the production of C5a and C5b-9 through the cleavage of C3. These studies have also defined an important role for C3 synthesized within ischemic kidney. Less clear however is the mechanism of complement activation that leads to the cleavage of C3 in ischemic tissues and to what extent the potential trigger mechanisms are organ dependent - an important question which informs the development of therapies that are more selective in their ability to limit the injury, yet preserve the other functions of complement where possible. Here we consider recent evidence for each of the three major pathways of complement activation (classical, lectin, and alternative) as mediators of I/R injury, and in particular highlight the role of lectin molecules that increasingly seem to underpin the injury in different organ models and in addition reveal unusual routes of complement activation that contribute to organ damage.

History

Citation

Frontiers in Immunology, 2012, 3, pp. 341-?

Author affiliation

/Organisation/COLLEGE OF MEDICINE, BIOLOGICAL SCIENCES AND PSYCHOLOGY/School of Medicine/Department of Infection, Immunity and Inflammation

Version

VoR (Version of Record)

Published in

Frontiers in Immunology

eissn

1664-3224

Copyright date

2012

Available date

31/10/2016

Publisher version

http://journal.frontiersin.org/article/10.3389/fimmu.2012.00341/

Language

en

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