肺泡Ⅱ型上皮细胞衰老在特发性肺纤维化中的研究进展

Research progress of alveolar typeⅡepithelial cells senescence in idiopathic pulmonary fibrosis

细胞衰老是组织和器官衰老的原始动力和主要病源,也是特发性肺纤维化(IPF)发生、发展的关键,肺泡Ⅱ型上皮细胞(AT2)的衰老是IPF的重要驱动因素之一。AT2衰老所致的衰老相关分化障碍可导致AT2分化停滞及肺纤维化的反分化,在其分泌的衰老相关分泌表型创造的低炎环境下协同促进了IPF的发生、发展。因此,预防AT2衰老或靶向清除衰老的AT2、阻断衰老相关分泌表型的分泌可能会对IPF的治疗提供思路。

Cellular senescence is the primary driving force and main pathogenesis of tissue and organ senescence,and it is also the key to the occurrence and development of idiopathic pulmonary fibrosis(IPF).AT2 senescence is one of the most important driving factors of IPF.AT2 senescence induced senescence-associated differentiation disorder can cause AT2 differentiation arrest and trans-differentiation of pulmonary fibrosis,which synergistically promotes the occurrence and development of IPF under the senescence-associated low-grade inflammation environment created by the senescence-associated secretory phenotype secreted by AT2.Therefore,preventing AT2 senescence or targeting the elimination of senescent AT2 and blocking senescence-associated secretory phenotype secretion may provide new ideas for the treatment of IPF.