转录组
氧化应激
疾病
背景(考古学)
肺
细胞外基质
生物
特发性肺纤维化
纤维化
肺纤维化
免疫学
基因表达
病理
基因
医学
遗传学
内科学
内分泌学
古生物学
作者
Evan A. Elko,James Mahoney,Pamela M. Vacek,Albert van der Vliet,Vikas Anathy,Jos van der Velden,Yvonne M. W. Janssen‐Heininger,David J. Seward
标识
DOI:10.1016/j.freeradbiomed.2019.07.011
摘要
Aging is associated with enhanced oxidative stress and increased susceptibility to numerous diseases. This relationship is particularly striking with respect to the incidence of fibrotic lung disease. To identify potential mechanisms underlying the association between aging and susceptibility to fibrotic lung disease we analyzed transcriptome data from 342 disease-free human lung samples as a function of donor age. Our analysis reveals that aging in lung is accompanied by modest yet progressive changes in genes modulating redox homeostasis, the TGF-beta 1 signaling axis, and the extracellular matrix (ECM), pointing to an aging lung functional network (ALFN). Further, the transcriptional changes we document are tissue-specific, with age-dependent gene expression patterns differing across organ systems. Our findings suggest that the age-associated increased incidence of fibrotic pulmonary disease occurs in the context of tissue-specific, age-dependent transcriptional changes. Understanding the relationship between age-associated gene expression and susceptibility to fibrotic pulmonary disease may allow for more accurate risk stratification and effective therapeutic interventions within this challenging clinical space.
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