Mechanisms of lung ischemia-reperfusion injury.
Mechanisms of lung ischemia-reperfusion injury.
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DOI：
10.1097/mot.0000000000000304
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发表时间：
2016-06
影响因子：
2.2
通讯作者：
Sharma AK
中科院分区：
文献类型：
--
作者：
Laubach VE;Sharma AK
肺非常容易受到损伤，尽管在外科治疗和免疫抑制方面取得了进展，但肺移植的结果是任何实体器官移植中最差的。肺移植的成功受到因缺血再灌注（IR）损伤（以强烈炎症、肺泡损伤和血管渗透性为特征）而导致的原发性移植物功能障碍（PGD）发生率高的限制。本文就肺缺血再灌注损伤的主要机制作一综述。在过去的18个月里，许多研究描述了在实验环境中限制肺IR损伤的策略，这些策略通常揭示了机械的见解。这些策略中的许多涉及使用各种抗氧化剂、抗炎剂、间充质干细胞和气体分子通气。在理解先天免疫细胞活化、中性粒细胞浸润、内皮屏障功能障碍和氧化应激反应的机制方面取得了进一步的进展。肺移植后PGD的预防方法是迫切需要的，了解IR损伤的机制是开发新的和有效的治疗方法的关键。这样做，肺移植受者的急性和慢性结果都将得到显着改善。
Lungs are extremely susceptible to injury, and despite advances in surgical management and immunosuppression, outcomes for lung transplantation are the worst of any solid organ transplant. The success of lung transplantation is limited by high rates of primary graft dysfunction (PGD) due to ischemia-reperfusion (IR) injury characterized by robust inflammation, alveolar damage and vascular permeability. This review will summarize major mechanisms of lung IR injury with a focus on the most recent findings in this area. Over the past 18 months numerous studies have described strategies to limit lung IR injury in experimental settings, which often reveal mechanistic insight. Many of these strategies involved the use of various anti-oxidants, anti-inflammatory agents, mesenchymal stem cells, and ventilation with gaseous molecules. Further advancements have been achieved in understanding mechanisms of innate immune cell activation, neutrophil infiltration, endothelial barrier dysfunction, and oxidative stress responses. Methods for prevention of PGD after lung transplant are urgently needed, and understanding mechanisms of IR injury is critical for the development of novel and effective therapeutic approaches. In doing so, both acute and chronic outcomes of lung transplant recipients will be significantly improved.