Age-dependent dysregulation of redox genes may contribute to fibrotic pulmonary disease susceptibility.

ABSTRACT: 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 or

SUBMITTER: Elko EA 

PROVIDER: S-EPMC6820706 | biostudies-literature | 2019 Sep

REPOSITORIES: biostudies-literature