机械通气使用不当可引起或加重肺损伤，称为呼吸机所致肺损伤（ventilator‑induced lung injury, VILI），机械通气导致的肺纤维化则是VILI中非常严重的一种。文章综述机械通气引起肺纤维化的可能机制，肺泡上皮细胞及肺血管内皮细胞转化为间充质细胞，巨噬细胞极化及肥大细胞产生胶原、类胰蛋白酶等，都参与机械通气诱发的肺纤维化；汇总了NOD样受体热蛋白结构域相关蛋白3（NOD‑like receptor thermal protein domain associated protein 3, NLRP3）炎症小体、透明质酸（hyaluronic acid, HA）、中期因子（midkine, MK）、转化生长因子β（transforming growth factor‑β, TGF‑β）等细胞因子及Wnt等信号通路在机械通气肺纤维化中发挥的作用。文章多方面探索机械通气诱发肺纤维化的机制，为早期诊断及防治提供新思路。
Recent studies have shown that improper use of mechanical ventilation can cause or aggravate lung injury, known as mechanical ventilator‑associated lung injury (VILI). Pulmonary fibrosis caused by mechanical ventilation is severe in VILI. This paper reviews the possible mechanisms of pulmonary fibrosis induced by mechanical ventilation, including the transformation of alveolar epithelial cells and pulmonary vascular endothelial cells into mesenchymal cells, the excessive polarization of macrophages, and the production of collagen and trypsin‑like cells by mast cells, all of which are involved in the pulmonary fibrosis induced by mechanical ventilation. In this paper, we summarized the roles of NOD‑like receptor thermal protein domain associated protein 3 (NLRP3) inflammatory bodies, hyaluronic acid (HA), midkine (MK), transforming growth factor‑β (TGF‑β), and other cytokines as well as Wnt signaling pathways in mechanical ventilation of pulmonary fibrosis. Exploring the mechanism of pulmonary fibrosis induced by mechanical ventilation in various aspects provides new ideas for early diagnosis and prevention.
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