Idiopathic pulmonary fibrosis (IPF) is a progressive fatal lung disorder with an unknown etiology and very limited therapeutic options. The incidence and severity of IPF increase with advanced age, suggesting that aging is a major risk factor for IPF. The mechanism underlying the aging-related susceptibility to IPF, however, remains unclear. Cellular senescence, a permanent arrest of cell growth, has been increasingly recognized as an important contributor to aging and aging-related diseases, including IPF. Senescent cells have been identified in IPF lungs and in experimental lung fibrosis models. Removal of senescent cells pharmacologically or genetically improves lung function and reverses pulmonary fibrosis induced by different stimuli in experimental fibrosis models. Treatment with senolytic drugs also improves clinical symptoms in IPF patients. These intriguing findings suggest that cellular senescence contributes importantly to the pathogenesis of fibrotic lung diseases and targeting senescent cells may represent a novel approach for the treatment of fibrotic lung disorders. In this mini review, we summarize the recent advance in the field regarding the role of cellular senescence in fibrotic lung diseases, with a focus on IPF.

特发性肺纤维化（IPF）是一种进行性致命性肺部疾病，病因不明，治疗选择非常有限。 IPF 的发病率和严重程度随着年龄的增长而增加，表明衰老是 IPF 的主要危险因素。然而，与衰老相关的 IPF 易感性的潜在机制仍不清楚。细胞衰老（细胞生长的永久停滞）已被越来越多地认为是导致衰老和衰老相关疾病（包括 IPF）的重要因素。已在 IPF 肺部和实验性肺纤维化模型中鉴定出衰老细胞。在实验性纤维化模型中，通过药理学或遗传学去除衰老细胞可以改善肺功能并逆转由不同刺激引起的肺纤维化。使用 senolytic 药物治疗还可改善 IPF 患者的临床症状。这些有趣的发现表明，细胞衰老对纤维化肺部疾病的发病机制有重要影响，针对衰老细胞可能代表一种治疗纤维化肺部疾病的新方法。在这篇小综述中，我们总结了细胞衰老在纤维化肺疾病中的作用领域的最新进展，重点是 IPF。