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缺血与再灌注:从机制到转化。

Ischemia and reperfusion--from mechanism to translation.

机构信息

Department of Anesthesiology, Mucosal Inflammation Program, University of Colorado, Aurora, Colorado, USA.

出版信息

Nat Med. 2011 Nov 7;17(11):1391-401. doi: 10.1038/nm.2507.

DOI:10.1038/nm.2507
PMID:22064429
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3886192/
Abstract

Ischemia and reperfusion-elicited tissue injury contributes to morbidity and mortality in a wide range of pathologies, including myocardial infarction, ischemic stroke, acute kidney injury, trauma, circulatory arrest, sickle cell disease and sleep apnea. Ischemia-reperfusion injury is also a major challenge during organ transplantation and cardiothoracic, vascular and general surgery. An imbalance in metabolic supply and demand within the ischemic organ results in profound tissue hypoxia and microvascular dysfunction. Subsequent reperfusion further enhances the activation of innate and adaptive immune responses and cell death programs. Recent advances in understanding the molecular and immunological consequences of ischemia and reperfusion may lead to innovative therapeutic strategies for treating patients with ischemia and reperfusion-associated tissue inflammation and organ dysfunction.

摘要

缺血再灌注引起的组织损伤是多种疾病(包括心肌梗死、缺血性中风、急性肾损伤、创伤、心脏停搏、镰状细胞病和睡眠呼吸暂停)发病率和死亡率的主要原因。缺血再灌注损伤也是器官移植以及心胸、血管和普通外科手术中的一个主要挑战。在缺血器官内,代谢供需之间的失衡导致严重的组织缺氧和微血管功能障碍。随后的再灌注进一步增强了固有和适应性免疫反应以及细胞死亡程序的激活。目前对缺血和再灌注引起的分子和免疫学后果的认识的进展,可能为治疗与缺血和再灌注相关的组织炎症和器官功能障碍的患者提供创新性的治疗策略。

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The immunology of stroke: from mechanisms to translation.中风的免疫学:从机制到转化。
Nat Med. 2011 Jul 7;17(7):796-808. doi: 10.1038/nm.2399.
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