PDF(Pubmed)
Abstract：
UNASSIGNED: Idiopathic pulmonary fibrosis (IPF) is a chronic progressive interstitial pneumonia of unknown etiology. An increasing number of studies have reported that the incidence of IPF increases with age. Simultaneously, the number of senescent cells increased in IPF. Epithelial cell senescence, an important component of epithelial cell dysfunction, plays a key role in IPF pathogenesis. This article summarizes the molecular mechanisms associated with alveolar epithelial cell senescence and recent advances in the applications of drugs targeting pulmonary epithelial cell senescence to explore novel therapeutic approaches for the treatment of pulmonary fibrosis.
UNASSIGNED: All literature published in English on PubMed, Web of Science, and Google Scholar were electronically searched online using the following keyword combinations: aging, alveolar epithelial cell, cell senescence, idiopathic pulmonary fibrosis, WNT/β-catenin, phosphatidylinositol-3-kinase/protein kinase B (PI3K/Akt), mammalian target of rapamycin (mTOR), and nuclear factor kappa B (NF-κB).
UNASSIGNED: We focused on signaling pathways associated with alveolar epithelial cell senescence in IPF, including WNT/β-catenin, PI3K/Akt, NF-κB, and mTOR signaling pathways. Some of these signaling pathways are involved in alveolar epithelial cell senescence by affecting cell cycle arrest and secretion of senescence-associated secretory phenotype-associated markers. We also found that changes in lipid metabolism in alveolar epithelial cells can be induced by mitochondrial dysfunction, both of which contribute to cellular senescence and development of IPF.
UNASSIGNED: Decreasing senescent alveolar epithelial cells may be a promising strategy for the treatment of IPF. Therefore, further investigations into new treatments of IPF by applying inhibitors of relevant signaling pathways, as well as senolytic drugs, are warranted.
UNASSIGNED: All literature published in English on PubMed, Web of Science, and Google Scholar were electronically searched online using the following keyword combinations: aging, alveolar epithelial cell, cell senescence, idiopathic pulmonary fibrosis, WNT/β-catenin, phosphatidylinositol-3-kinase/protein kinase B (PI3K/Akt), mammalian target of rapamycin (mTOR), and nuclear factor kappa B (NF-κB).
UNASSIGNED: We focused on signaling pathways associated with alveolar epithelial cell senescence in IPF, including WNT/β-catenin, PI3K/Akt, NF-κB, and mTOR signaling pathways. Some of these signaling pathways are involved in alveolar epithelial cell senescence by affecting cell cycle arrest and secretion of senescence-associated secretory phenotype-associated markers. We also found that changes in lipid metabolism in alveolar epithelial cells can be induced by mitochondrial dysfunction, both of which contribute to cellular senescence and development of IPF.
UNASSIGNED: Decreasing senescent alveolar epithelial cells may be a promising strategy for the treatment of IPF. Therefore, further investigations into new treatments of IPF by applying inhibitors of relevant signaling pathways, as well as senolytic drugs, are warranted.
摘要：
UNASSIGNED：特发性肺纤维化（IPF）是一种病因不明的慢性进行性间质性肺炎。越来越多的研究报道IPF的发病率随着年龄的增长而增加。同时,IPF中衰老细胞数量增加。上皮细胞衰老,上皮细胞功能障碍的重要组成部分，在IPF发病机制中起关键作用。本文综述了肺泡上皮细胞衰老的相关分子机制以及靶向肺上皮细胞衰老的药物应用的最新进展，以探索治疗肺纤维化的新方法。
UASSIGNED：所有文献在PubMed上以英文出版，WebofScience,和谷歌学者使用以下关键字组合在网上进行电子搜索：老化，肺泡上皮细胞，细胞衰老,特发性肺纤维化,WNT/β-连环蛋白，磷脂酰肌醇-3-激酶/蛋白激酶B(PI3K/Akt),哺乳动物雷帕霉素靶蛋白（mTOR），核因子κB(NF-κB)。
UNASSIGNED：我们关注与IPF中肺泡上皮细胞衰老相关的信号通路，包括WNT/β-catenin，PI3K/Akt,NF-κB,和mTOR信号通路。这些信号通路中的一些通过影响细胞周期停滞和分泌与衰老相关的分泌表型相关的标志物而参与肺泡上皮细胞衰老。我们还发现肺泡上皮细胞脂质代谢的变化可以由线粒体功能障碍引起，两者都有助于IPF的细胞衰老和发育。
UNASSIGNED：减少衰老的肺泡上皮细胞可能是治疗IPF的一个有希望的策略。因此,通过应用相关信号通路的抑制剂进一步研究IPF的新疗法，以及抗衰老药物，是有保证的。
UASSIGNED：所有文献在PubMed上以英文出版，
UNASSIGNED：我们关注与IPF中肺泡上皮细胞衰老相关的信号通路，
UNASSIGNED：减少衰老的肺泡上皮细胞可能是治疗IPF的一个有希望的策略。
