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

摘要: Abstract Aging is associated with enhanced oxidative stress and increased susceptibility to numerous diseases. This relationship particularly striking respect the incidence of fibrotic lung disease. To identify potential mechanisms underlying association between aging disease we analyzed transcriptome data from 342 disease-free human samples as a function donor age. Our analysis reveals that in accompanied by modest yet progressive changes genes modulating redox homeostasis, TGF-beta 1 signaling axis, extracellular matrix (ECM), pointing an functional network (ALFN). Further, transcriptional document are tissue-specific, age-dependent gene expression patterns differing across organ systems. findings suggest age-associated pulmonary occurs context changes. Understanding may allow for more accurate risk stratification effective therapeutic interventions within this challenging clinical space.