细胞衰老参与特发性肺纤维化分子发病机制的最新研究进展

Latest advances on cell aging involved in molecular pathogenesis of idiopathic pulmonary fibrosis

特发性肺纤维化是一种不可逆、日益严重的间质性肺疾病,随着年龄的增长其发病率亦增加,此前已有学者证明细胞衰老参与特发性肺纤维化的发生。细胞衰老在机体中时刻发生,复制性衰老是一种生理活动,于机体有益,而过早性衰老却可导致包括肺的各个器官发生病变。活性氧自由基的产生、抑癌基因的失活、辐射以及各种细胞因子和细胞信号转导等因素均可激发细胞过早性衰老,衰老细胞可分泌多种细胞因子作用于衰老细胞本身或周围其他细胞,从而改变衰老细胞及其微环境。文章主要就端粒缩短、线粒体功能障碍、抑癌基因的失活、电离辐射等因素导致细胞过早性衰老的发生进行具体分析,阐明其导致细胞衰老发生的具体机制,以及这些因素如何参与特发性肺纤维化的发生发展进行系统总结。

Idiopathic pulmonary fibrosis is an irreversible and severe interstitial lung disease and its incidence increases with age.Previous studies have shown that cell aging is involved in its occurrence.Cell aging occurs every second and replicative aging is a physiological activity that benefits our body.Premature aging,however,contributes to the pathological changes in organs such as lung.Risk factors such as generation of reactive oxygen species,inactivation of tumor suppressor genes,radiation,and cytokines and cell signal transduction can stimulate premature aging of cells.Aging cells secrete a variety of cytokines to act on themselves or other surrounding cells,thus altering their microenvironment.This paper mainly analyzes the occurrence of cell premature aging caused by telomere shortening,mitochondrial dysfunction,inactivation of tumor suppressor gene and ionizing radiation,elucidates the specific mechanism,and systematically summarizes how these factors participate in the occurrence and development of idiopathic pulmonary fibrosis.