Liu Suqi, Xi Qian, Li Xuannian, Liu Huaman
The First College of Clinical Medicine, Shandong University of Traditional Chinese Medicine, Jinan, Shandong, China.
Six Sections of Geriatrics, Affiliated Hospital of Shandong University of Traditional Chinese Medicine, Jinan, Shandong, China.
Front Cell Dev Biol. 2025 Mar 31;13:1535601. doi: 10.3389/fcell.2025.1535601. eCollection 2025.
Idiopathic pulmonary fibrosis (IPF) is a chronic respiratory disease with an unknown origin and complex pathogenic mechanisms. A deeper understanding of these mechanisms is essential for effective treatment. Pulmonary fibrosis is associated with the senescence of alveolar type II epithelial (ATⅡ) cells. Additionally, ATⅡ senescence can lead to a senescence-associated secretory phenotype, which affects cellular communication and disrupts lung tissue repair, contributing to the development of IPF. The role of mitochondrial dysfunction in senescence-related diseases is increasingly recognized. It can induce ATⅡ senescence through apoptosis, impaired autophagy, and disrupted energy metabolism, potentially playing a key role in IPF progression. This article explores the therapeutic potential of targeting cellular senescence and mitochondrial dysfunction, emphasizing their significant roles in IPF pathogenesis.
特发性肺纤维化（IPF）是一种病因不明、发病机制复杂的慢性呼吸系统疾病。深入了解这些机制对于有效治疗至关重要。肺纤维化与II型肺泡上皮（ATⅡ）细胞衰老有关。此外，ATⅡ衰老可导致衰老相关分泌表型，影响细胞间通讯并破坏肺组织修复，促使IPF的发展。线粒体功能障碍在衰老相关疾病中的作用日益受到认可。它可通过凋亡、自噬受损和能量代谢紊乱诱导ATⅡ衰老，可能在IPF进展中起关键作用。本文探讨了针对细胞衰老和线粒体功能障碍的治疗潜力，强调了它们在IPF发病机制中的重要作用。
