Which pathways trigger the role of complement in ischaemia/reperfusion injury?
Which pathways trigger the role of complement in ischaemia/reperfusion injury?
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DOI：
10.3389/fimmu.2012.00341
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发表时间：
2012
影响因子：
7.3
通讯作者：
Sacks SH
中科院分区：
文献类型：
--
作者：
Farrar CA;Asgari E;Schwaeble WJ;Sacks SH
对补体在缺血/再灌注 (I/R) 损伤中的作用的研究已经确定了依赖于通过 C3 裂解产生 C5a 和 C5b-9 的常见效应机制。这些研究还明确了缺血肾脏内合成的 C3 的重要作用。然而，不太清楚的是补体激活机制导致缺血组织中 C3 裂解，以及潜在的触发机制在多大程度上是器官依赖性的——这是一个重要的问题，它为开发更具选择性的限制损伤的能力，同时尽可能保留补体的其他功能的疗法提供了信息。在这里，我们考虑了补体激活的三种主要途径（经典、凝集素和替代）作为 I/R 损伤介质的最新证据，特别强调了凝集素分子的作用，它们似乎越来越多地支持不同器官模型中的损伤，此外还揭示了导致器官损伤的补体激活的不寻常途径。
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.
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影响因子：
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