机械牵张诱导肺上皮细胞转化——肺纤维增殖的新机制

New mechanism of pulmonary fibro-proliferafion： the epithelial-mesenchymal transition induced by mechanical stress

背景机械通气是纠正低氧血症的重要治疗手段之一，在急性呼吸窘迫综合征（acute respiratory distress syndrome，ARDS）的支持措施中拥有无可替代的地位。但机械通气治疗在提供有效呼吸支持治疗的同时，还可能导致或进一步加重肺损伤甚至引起肺部纤维化。有研究报道，在ARDS致死原因中，难以控制的肺纤维化占40％～70％。目的就机械性牵拉致肺纤维化的发生机制的最新研究进行综述，以期人们深化对肺纤维化发生机制的认识。内容机械通气对肺组织产生的机械牵拉作用可诱导肺上皮细胞表型转化，这是形成肺纤维化的重要基础。趋向一系列刺激因素均可诱发肺纤维化，包括致敏源、化学毒素和机械牵拉等。而机械牵拉导致的肺纤维化已成为重症监护过程中的重要致死原因之一，这就需要我们的高度重视，在充分了解其发病机制的基础上，研究出有效的预防和干预措施。

Background Mechanical ventilation is one of the most significant therapeutic strategies of mitigating hypoxla, which has become essential for the support of acute respiratory distress syndrome patient. However, it can induce or aggravate ventilator-associated lung injury, even leading to pulmonary fibrosis. It is reported that the mortality of acute respiratory distress syndrome （ARDS） caused by uncontrollable pulmonary fibrosis ranges 40% from 70%. Objective There is a intimate relationship between pulmonary fibro-proliferation and epithelial-mesenchymal transition （EMT） induced by mechanical stress. Content This article reviews the latest advances on the mechanism of pulmonary fibrosis caused by mechanical stretch in order to deepen the understanding of the pathogenesis of pulmonary fibrosis. Trend The causality of pulmonary fibrotic disease is varied, with an array of triggers including allergens, chemicals and mechanical stress. During intensive care unit stay, mechanical stress has become one of the most significant causes of pulmonary fibrosis with high mortality, which requires us to investigate integrating mechanisms of pulmonary fibrosis and intervention of this fibrotic disease.