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急性呼吸窘迫综合征:从机制到转化

The acute respiratory distress syndrome: from mechanism to translation.

作者信息

Han SeungHye, Mallampalli Rama K

机构信息

Division of Pulmonary, Allergy, and Critical Care Medicine, Department of Medicine, Acute Lung Injury Center of Excellence, University of Pittsburgh, Pittsburgh, PA 15213;

Division of Pulmonary, Allergy, and Critical Care Medicine, Department of Medicine, Acute Lung Injury Center of Excellence, University of Pittsburgh, Pittsburgh, PA 15213; Department of Cell Biology and Physiology, University of Pittsburgh, Pittsburgh, PA 15213; and Medical Specialty Service Line, Veterans Affairs Pittsburgh Healthcare System, Pittsburgh, PA 15240

出版信息

J Immunol. 2015 Feb 1;194(3):855-60. doi: 10.4049/jimmunol.1402513.

DOI:10.4049/jimmunol.1402513
PMID:25596299
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4299926/
Abstract

The acute respiratory distress syndrome (ARDS) is a form of severe hypoxemic respiratory failure that is characterized by inflammatory injury to the alveolar capillary barrier, with extravasation of protein-rich edema fluid into the airspace. Although many modalities to treat ARDS have been investigated over the past several decades, supportive therapies remain the mainstay of treatment. In this article, we briefly review the definition, epidemiology, and pathophysiology of ARDS and present emerging aspects of ARDS pathophysiology that encompass modulators of the innate immune response, damage signals, and aberrant proteolysis that may serve as a foundation for future therapeutic targets.

摘要

急性呼吸窘迫综合征(ARDS)是一种严重的低氧性呼吸衰竭形式,其特征是肺泡毛细血管屏障发生炎性损伤,富含蛋白质的水肿液渗入气腔。尽管在过去几十年中已经研究了许多治疗ARDS的方法,但支持性治疗仍然是主要的治疗手段。在本文中,我们简要回顾了ARDS的定义、流行病学和病理生理学,并介绍了ARDS病理生理学的新进展,包括固有免疫反应调节剂、损伤信号和异常蛋白水解,这些可能为未来的治疗靶点奠定基础。

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