Specialized Pro-resolving Mediators Regulate Alveolar Fluid Clearance during Acute Respiratory Distress Syndrome.

Specialized Pro-resolving Mediators Regulate Alveolar Fluid Clearance during Acute Respiratory Distress Syndrome.
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急性呼吸窘迫综合征期间专门的促缓解介质调节肺泡液体清除。

DOI:
10.4103/0366-6999.229890
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发表时间:
2018-04-20
影响因子:
6.1
通讯作者:
Jin SW
Jin SW
中科院分区:
医学2区
文献类型:
--
作者:
Wang Q;Yan SF;Hao Y;Jin SW

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急性呼吸窘迫综合征(ARDS)是一种急性致死性临床综合征,其特征是肺泡上皮损伤,损害肺部主动液体运输,并阻碍肺泡腔水肿液的重吸收。本综述旨在讨论促缓解介质在 ARDS 肺泡液清除率 (AFC) 调节中的作用。截至 2017 年 9 月发表的文章选自 PubMed,关键词为“肺泡液清除”或“肺水肿”或“急性肺损伤”或“急性呼吸窘迫综合征”,以及“专门的促溶解介质”或“脂氧素”或“溶解素”或“保护素”或“maresin”或“肺泡上皮细胞”或“阿司匹林触发的脂质介质”或“一氧化碳和血红素加氧酶”或“膜联蛋白 A1”。我们纳入了截至 2017 年 9 月发表的所有相关文章,研究设计没有限制。特殊促解介质(SPM)作为促炎介质,不仅上调上皮钠通道、Na,K-ATP酶、囊性纤维化跨膜电导调节因子(CFTR)和水通道蛋白水平,而且提高Na,K-ATP酶活性以促进ARDS中的AFC。除了对肺泡上皮的离子通道和泵产生直接影响外,SPM 还抑制炎症细胞因子的表达并改善肺泡上皮细胞的修复,从而增强 ARDS 中的 AFC。本综述讨论了肺水肿液体重吸收的新机制。 SPM 可能为设计高精度控制 ALI/ARDS 的“重吸收靶向”疗法提供新的机会。
Acute respiratory distress syndrome (ARDS) is an acute and lethal clinical syndrome that is characterized by the injury of alveolar epithelium, which impairs active fluid transport in the lung, and impedes the reabsorption of edema fluid from the alveolar space. This review aimed to discuss the role of pro-resolving mediators on the regulation of alveolar fluid clearance (AFC) in ARDS. Articles published up to September 2017 were selected from the PubMed, with the keywords of “alveolar fluid clearance” or “lung edema” or “acute lung injury” or “acute respiratory distress syndrome”, and “specialized pro-resolving mediators” or “lipoxin” or “resolvin” or “protectin” or “maresin” or “alveolar epithelial cells” or “aspirin-triggered lipid mediators” or “carbon monoxide and heme oxygenase” or “annexin A1”. We included all relevant articles published up to September 2017, with no limitation of study design. Specialized pro-resolving mediators (SPMs), as the proinflammatory mediators, not only upregulated epithelial sodium channel, Na,K-ATPase, cystic fibrosis transmembrane conductance regulator (CFTR), and aquaporins levels, but also improved Na,K-ATPase activity to promote AFC in ARDS. In addition to the direct effects on ion channels and pumps of the alveolar epithelium, the SPMs also inhibited the inflammatory cytokine expression and improved the alveolar epithelial cell repair to enhance the AFC in ARDS. The present review discusses a novel mechanism for pulmonary edema fluid reabsorption. SPMs might provide new opportunities to design “reabsorption-targeted” therapies with high degrees of precision in controlling ALI/ARDS.
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