Han Shan, Lu Qiangwei, Liu Xiaoqiu
Department of Respiratory and Critical Care Medicine, The Second Hospital of Jilin University, Changchun, Jilin 130000, P.R. China.
Department of Respiratory and Critical Care Medicine, Affiliated Hospital of Shaanxi University of Traditional Chinese Medicine, Xianyang, Shaanxi 712000, P.R. China.
Exp Ther Med. 2023 Feb 15;25(4):145. doi: 10.3892/etm.2023.11844. eCollection 2023 Apr.
Idiopathic pulmonary fibrosis (IPF) is a progressive, irreversible and fatal interstitial lung disease of unknown cause, with a median survival of 2-3 years. Its pathogenesis is unclear and there is currently no effective treatment for IPF. Approximately two-thirds of patients with IPF are >60 years old, with a mean age of 66 years, suggesting a link between aging and IPF. However, the mechanism by which aging promotes development of PF remains unclear. Senescence of alveolar epithelial cells and lung fibroblasts (LFs) and their senescence-associated secretion phenotype (SASP) may be involved in the occurrence and development of IPF. The present review focus on senescence of LFs and epithelial and stem cells, as well as SASP, the activation of profibrotic signaling pathways and potential treatments for pathogenesis of IPF.
特发性肺纤维化(IPF)是一种病因不明的进行性、不可逆且致命的间质性肺疾病,中位生存期为2至3年。其发病机制尚不清楚,目前尚无针对IPF的有效治疗方法。大约三分之二的IPF患者年龄超过60岁,平均年龄为66岁,提示衰老与IPF之间存在关联。然而,衰老促进肺纤维化发展的机制仍不清楚。肺泡上皮细胞和肺成纤维细胞(LFs)的衰老及其衰老相关分泌表型(SASP)可能参与IPF的发生和发展。本综述重点关注LFs、上皮细胞和干细胞的衰老,以及SASP、促纤维化信号通路的激活和IPF发病机制的潜在治疗方法。