Molecular Biology Ying Yang in Alveolar Fluid Clearance.
Molecular Biology Ying Yang in Alveolar Fluid Clearance.
复制标题
肺泡液清除中的分子生物学阴阳。
DOI：
10.1097/ccm.0000000000001238
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发表时间：
2015
影响因子：
8.8
通讯作者：
Zimmerman,JerryJ
中科院分区：
文献类型：
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作者：
Zimmerman,JerryJ
护理医学需要相当多的关注。然而，在缩写、双重否定和信号通路复杂性的字母汤中，提供了新的信息，最终可能为我们理解和治疗急性呼吸窘迫综合征(ARDS)的临床方法提供信息。正如作者在导言部分指出的那样，ARDS相关的急性肺水肿不仅是弥漫性肺毛细血管渗漏的一种功能，也是肺泡液清除受损的一种功能。ARDS的治疗在很大程度上是支持性的，在提供机械通风和避免肺部修复时液体超载方面。目前尚不清楚在这种情况下使用皮质类固醇干预是否有益(2，3)。尽管这项研究完全是基础科学，但Lin等人的研究(1)鼓励我们推测，调节肺泡液清除可能是对ARDS的另一种治疗干预。在他们的研究中，作者利用了一种小鼠高氧暴露肺损伤模型，该模型可重复性地导致急性缺氧性呼吸衰竭合并肺水肿。一开始，了解正在研究的分子组成是很重要的。无赖氨酸激酶(WNK)是目前研究的热点。尽管WNK自身的激活尚不清楚，但本研究检测了WNK下游通路，该通路涉及另一种称为STE20/SPS1相关的富含脯氨酸/丙氨酸的激酶(SPAK)的磷酸化，进而激活钠-氯化钾共转运体(NKCC)。作者指出，
Care Medicine required considerable focus. However, amidst the alphabet soup of abbreviations, double negatives, and signaling pathway complexity lays novel information that ultimately may inform our clinical approach to understanding and treating acute respiratory distress syndrome (ARDS). As the authors point out in their introductory section, ARDS-associated acute pulmonary edema is a function not only of diffuse pulmonary capillary leak but also of impaired alveolar fluid clearance. Treatment of ARDS has largely been supportive in terms of providing mechanical ventilation and avoidance of fluid overload while the lungs undergo repair. It remains unclear if intervention with corticosteroids is beneficial in this setting (2, 3). Although completely basic science in its conduct, the study by Lin et al (1) encourages us to speculate that modulation of alveolar fluid clearance may represent another therapeutic intervention for ARDS.In their investigation, the authors utilized a murine hyperoxia-exposure lung injury model that reproducibly results in acute hypoxemic respiratory failure associated with pulmonary edema. At the onset, it is important to understand the molecular components being investigated. With-no-lysine-kinase (WNK) is the focus of investigation. Although its own activation remains somewhat unclear, this investigation examined the WNK downstream pathway that involves phosphorylation of another kinase termed STE20/SPS1-related proline/alanine-rich kinase (SPAK) and in turn phosphorylation activation of the sodium-potassiumchloride cotransporter (NKCC). The authors point out that