Idiopathic pulmonary fibrosis (IPF) is a progressive disease characterised by an inexorable decline in lung function. The development of IPF involves multiple positive feedback loops; and a strong support role of the Hippo/YAP signalling pathway, which is essential for regulating cell proliferation and organ size, in IPF pathogenesis has been unveiled recently in cell and animal models. YAP/TAZ contributes to both pulmonary fibrosis and alveolar regeneration via the conventional Hippo/YAP signalling pathway, G protein-coupled receptor signalling, and mechanotransduction. Selectively inhibiting YAP/TAZ in lung fibroblasts may inhibit fibroblast proliferation and extracellular matrix deposition, while activating YAP/TAZ in alveolar epithelial cells may promote alveolar regeneration. In this review, we explore, for the first time, the bidirectional and cell-specific regulation of the Hippo/YAP pathway in IPF pathogenesis and discuss recent research progress and future prospects of IPF treatment based on Hippo/YAP signalling, thus providing a basis for the development of new therapeutic strategies to alleviate or even reverse IPF.

特发性肺纤维化 (IPF) 是一种进行性疾病，其特征是肺功能不可避免地下降。IPF的发展涉及多个正反馈循环；最近在细胞和动物模型中揭示了 Hippo/YAP 信号通路在 IPF 发病机制中的强大支持作用，该通路对调节细胞增殖和器官大小至关重要。YAP/TAZ 通过传统的 Hippo/YAP 信号通路、G 蛋白偶联受体信号和机械转导促进肺纤维化和肺泡再生。选择性抑制肺成纤维细胞中的YAP/TAZ可抑制成纤维细胞增殖和细胞外基质沉积，而激活肺泡上皮细胞中的YAP/TAZ可促进肺泡再生。在这篇评论中，我们第一次探索，