Ischemia/reperfusion injury: The role of immune cells.
Ischemia/reperfusion injury: The role of immune cells.
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DOI：
10.4330/wjc.v2.i10.325
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发表时间：
2010-10
影响因子：
1.9
通讯作者：
M. Zuidema;Cuihua Zhang
中科院分区：
文献类型：
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作者：
M. Zuidema;Cuihua Zhang
缺血/再灌注（I/R）损伤是一种以先天免疫和适应性免疫应答为特征的炎性病症。本文综述了I/R损伤中的急性炎症反应，以及慢性缺血性疾病中导致急性事件期间脆弱性增加的适应性免疫机制，与已被证明介导先天免疫的细胞类型有关，以适应性免疫反应在I/R中，特别是心肌梗死。新的方面也突出了在心血管系统内的机制和心血管危险因素，可能参与伴随心肌梗死的炎症反应。实验性心肌I/R表明免疫细胞可能介导再灌注损伤。具体而言，单核细胞，巨噬细胞，T细胞，肥大细胞，血小板和内皮细胞的补体级联反应，Toll样受体，细胞因子，氧化应激，肾素-血管紧张素系统，并在参考微血管系统的I/R的信号转导机制进行了讨论。最后，本综述中总结的数据结果对于可能转化为临床心脏病学实践和药物开发的可能途径最为重要。
Ischemia/reperfusion (I/R) injury is an inflammatory condition that is characterized by innate immunity and an adaptive immune response. This review is focused on the acute inflammatory response in I/R injury, and also the adaptive immunological mechanisms in chronic ischemic disease that lead to increased vulnerability during acute events, in relation to the cell types that have been shown to mediate innate immunity to an adaptive immune response in I/R, specifically myocardial infarction. Novel aspects are also highlighted in respect to the mechanisms within the cardiovascular system and cardiovascular risk factors that may be involved in the inflammatory response accompanying myocardial infarction. Experimental myocardial I/R has suggested that immune cells may mediate reperfusion injury. Specifically, monocytes, macrophages, T-cells, mast cells, platelets and endothelial cells are discussed with reference to the complement cascade, toll-like receptors, cytokines, oxidative stress, renin-angiotensin system, and in reference to the microvascular system in the signaling mechanisms of I/R. Finally, the findings of the data summarized in this review are most important for possible translation into clinical cardiology practice and possible avenues for drug development.