Age-dependent dysregulation of redox genes may contribute to fibrotic pulmonary disease susceptibility.
Free Radic Biol Med
; 141: 438-446, 2019 09.
Article
em En
| MEDLINE
| ID: mdl-31315063
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 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.
Palavras-chave
Texto completo:
1
Coleções:
01-internacional
Base de dados:
MEDLINE
Assunto principal:
Fibrose Pulmonar
/
Envelhecimento
/
Transcriptoma
/
Pneumopatias
Tipo de estudo:
Etiology_studies
/
Prognostic_studies
Limite:
Adult
/
Aged
/
Female
/
Humans
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Male
/
Middle aged
Idioma:
En
Revista:
Free Radic Biol Med
Assunto da revista:
BIOQUIMICA
/
MEDICINA
Ano de publicação:
2019
Tipo de documento:
Article
País de afiliação:
Estados Unidos