Balibrea Jose L, Arias-Díaz Javier
Department of Surgery, Hospital Clinico San Carlos, Universidad Complutense, 28040, Madrid, Spain.
World J Surg. 2003 Dec;27(12):1275-84. doi: 10.1007/s00268-003-7258-3. Epub 2003 Oct 28.
The acute respiratory distress syndrome (ARDS) is a process of acute inflammatory lung injury that affects a diverse array of surgical and medical patients. The syndrome is mediated by a complex and interacting system of chemical mediators produced by several types of pulmonary cells. Regardless of the predisposing causes, activation of the nuclear factor kappa B seems to be, at the molecular level, a signature event of ARDS, leading to the rapid activation of intracellular signaling pathways, which coordinate the induction of multiple genes encoding inflammatory mediators. There are at least two compelling reasons for promoting an understanding of these interactions and their molecular mediators and second messengers: new therapies intended to modulate these factors continue to be developed, and the levels of some of these molecules, most notably cytokines, may serve as early indicators of the onset of ARDS.
急性呼吸窘迫综合征(ARDS)是一种急性炎症性肺损伤过程,影响着众多外科和内科患者。该综合征由几种肺细胞产生的复杂且相互作用的化学介质系统介导。无论诱发原因如何,在分子水平上,核因子κB的激活似乎是ARDS的标志性事件,导致细胞内信号通路迅速激活,这些信号通路协调诱导多种编码炎症介质的基因。促进对这些相互作用及其分子介质和第二信使的理解有至少两个令人信服的理由:旨在调节这些因素的新疗法不断被开发,并且其中一些分子的水平,最显著的是细胞因子,可能作为ARDS发病的早期指标。