Jiang Mengna, Bu Wenxia, Wang Xuehai, Ruan Jialing, Shi Weijian, Yu Siqi, Huang Lizhen, Xue Peng, Tang Juan, Zhao Xinyuan, Su Liling, Cheng Demin
Department of Occupational Medicine and Environmental Toxicology, Nantong Key Laboratory of Environmental Toxicology, School of Public Health, Nantong University, Nantong, 226019, China.
Department of Clinical Medicine, Jiangxi Medical College, Shangrao, 334000, China.
J Transl Med. 2025 May 8;23(1):515. doi: 10.1186/s12967-025-06514-2.
Pulmonary fibrosis (PF) is a chronic, progressive interstitial lung disease characterized by excessive deposition of extracellular matrix (ECM) and abnormal fibroblast proliferation, which is mainly caused by air pollution, smoking, aging, occupational exposure, environmental pollutants exposure, and microbial infections. Although antifibrotic agents such as pirfenidone and nintedanib, approved by the United States (US) Food and Drug Administration (FDA), can slow the decline in lung function and disease progression, their side effects and delivery inefficiency limit the overall prognosis of PF. Therefore, there is an urgent need to develop effective therapeutic targets and delivery approaches for PF in clinical settings. This review provides an overview of the pathogenic mechanisms, therapeutic drug targeting signaling pathways, and promising drug delivery strategies for treating PF.
肺纤维化(PF)是一种慢性进行性间质性肺疾病,其特征是细胞外基质(ECM)过度沉积和成纤维细胞异常增殖,主要由空气污染、吸烟、衰老、职业暴露、环境污染物暴露和微生物感染引起。尽管美国食品药品监督管理局(FDA)批准的抗纤维化药物如吡非尼酮和尼达尼布可以减缓肺功能下降和疾病进展,但其副作用和给药效率低下限制了PF的总体预后。因此,临床迫切需要为PF开发有效的治疗靶点和给药途径。本综述概述了PF的致病机制、治疗药物靶向信号通路以及有前景的药物递送策略。