Huang Jingru, Qin Jianfeng, Zhu Yuguang, Shen Ao
Guangzhou Municipal and Guangdong Provincial Key Laboratory of Molecular Target and Clinical Pharmacology, NMPA and State Key Laboratory of Respiratory Disease, School of Pharmaceutical Sciences and the Fifth Affiliated Hospital, Guangzhou Medical University, Guangzhou, Guangdong, China.
Front Mol Biosci. 2025 Jul 17;12:1647300. doi: 10.3389/fmolb.2025.1647300. eCollection 2025.
Pulmonary fibrosis (PF) is a fatal disease characterized by progressive fibrosis of lung tissue, with a key pathological feature of excessive accumulation of extracellular matrix. PF occurs from complicated origins, while emerging findings have suggested the involvement of the environmental factors in the risk of PF through epigenetic regulation. This article will discuss how recent advances in epigenetic alterations of DNA methylation, RNA methylation, histone modifications, and non-coding RNAs contribute to PF development through molecular mechanisms and cellular processes, including fibroblast-to-myofibroblast transition (FMT), epithelial-to-mesenchymal transition (EMT), alveolar epithelial cell injury and immune cell interactions in the past 5 years.
肺纤维化（PF）是一种致命疾病，其特征为肺组织进行性纤维化，关键病理特征是细胞外基质过度积聚。PF病因复杂，而新出现的研究结果表明环境因素通过表观遗传调控参与PF发病风险。本文将探讨过去5年中DNA甲基化、RNA甲基化、组蛋白修饰和非编码RNA等表观遗传改变的最新进展如何通过分子机制和细胞过程，包括成纤维细胞向肌成纤维细胞转变（FMT）、上皮向间充质转变（EMT）、肺泡上皮细胞损伤和免疫细胞相互作用，促进PF的发展。
