Macrophage-mediated injury and repair after ischemic kidney injury.
Macrophage-mediated injury and repair after ischemic kidney injury.
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DOI：
10.1007/s00467-013-2726-y
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发表时间：
2015-02
影响因子：
3
通讯作者：
Cantley, Lloyd G.
中科院分区：
文献类型：
--
作者：
Huen, Sarah C.;Cantley, Lloyd G.
急性缺血性肾损伤是住院患者常见的并发症。目前还没有治疗方法可以增强肾脏修复或预防进行性肾纤维化。急性肾损伤的动物模型表明，先天免疫系统的激活在缺血/再灌注损伤的全身反应中起着重要作用。巨噬细胞耗竭研究表明，巨噬细胞作为先天免疫反应的关键参与者，在再灌注后增强初始损伤，但也促进肾小管修复，并参与缺血性损伤后的长期肾纤维化。缺血/再灌注损伤后不同时间点巨噬细胞消耗后的不同功能结果表明巨噬细胞激活状态存在异质性。因此，确定巨噬细胞激活转变的调控途径对于理解巨噬细胞介导的缺血后肾脏损伤和修复的调控机制至关重要。本文综述了我们目前对肾缺血/再灌注损伤后单核细胞募集、巨噬细胞激活和巨噬细胞效应功能的复杂和复杂控制途径的理解。仔细描述修复和溶解途径可以为开发有效的治疗方法提供治疗靶点，以提供急性肾损伤患者。
Acute ischemic kidney injury is a common complication in hospitalized patients. Currently no treatment is available for augmenting kidney repair or preventing progressive kidney fibrosis. Animal models of acute kidney injury demonstrate that activation of the innate immune system plays a major role in the systemic response to ischemia/reperfusion injury. Macrophage depletion studies suggest that macrophages, key participants in the innate immune response, augment the initial injury after reperfusion, but also promote tubular repair and contribute to long-term kidney fibrosis after ischemic injury. The distinct functional outcomes seen following macrophage depletion at different time points after ischemia/reperfusion injury suggest heterogeneity in macrophage activation states. Identifying the pathways that regulate the transitions of macrophage activation is thus critical for understanding the mechanisms that govern both macrophage-mediated injury and repair in the post-ischemic kidney. This review examines our current understanding of the complex and intricately controlled pathways that determine monocyte recruitment, macrophage activation, and macrophage effector functions after renal ischemia/reperfusion injury. Careful delineation of repair and resolution pathways could provide therapeutic targets for the development of effective treatments to offer patients with acute kidney injury.
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DOI：
10.1146/annurev-pathol-020712-163930
发表时间：
2013-01-24
期刊：
Annual review of pathology
影响因子：
--
作者：
Duffield JS;Lupher M;Thannickal VJ;Wynn TA
通讯作者：
Wynn TA
影响因子：
2.8
作者：
Bradford, Barry M.;Sester, David P.;Mabbott, Neil A.
通讯作者：
Mabbott, Neil A.
影响因子：
15.9
作者：
Fadok, VA;Bratton, DL;Henson, PM
通讯作者：
Henson, PM
影响因子：
6.1
作者：
Jo, SK;Sung, SA;Kim, HK
通讯作者：
Kim, HK
影响因子：
19.6
作者：
Ferenbach, David A.;Nkejabega, Noemie C. J.;Hughes, Jeremy
通讯作者：
Hughes, Jeremy