Abstract
Background: Circulating markers of oxidative stress have been associated with lower lung function. Our objective was to study the association of gene expression levels of oxidative stress pathway genes (ALOX12, ALOX15, ARG2, GSTT1, LPO, MPO, NDUFB3, PLA2G7, and SOD3) and lung function forced expiratory volume in one second (FEV1), forced vital capacity (FVC) in Coronary Artery Risk Development in Young Adults study. Methods: Lung function was measured using spirometry and the Nanostring platform was used to estimate gene expression levels. Linear regression models were used to study association of lung function measured at year 30, 10-year decline in lung function and gene expression after adjustment for center, smoking, and BMI, measured at year 25. Results: The 10-year decline of FEV1 was faster in highest NDUFB3 quartile compared to the lowest (difference = −2.09%; p = 0.001) after adjustment for multiple comparisons. The 10-year decline in FEV1 and FVC was nominally slower in highest versus lowest quartile of PLA2G7 (difference = 1.14%; p = 0.02, and difference = 1.06%; p = 0.005, respectively). The other genes in the study were not associated with FEV1 or FVC. Conclusion: Higher gene expression levels in oxidative stress pathway genes are associated with faster 10-year FEV1 decline.
Original language | English (US) |
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Article number | e1832 |
Journal | Molecular Genetics and Genomic Medicine |
Volume | 9 |
Issue number | 12 |
DOIs | |
State | Published - Dec 2021 |
Funding
The CARDIA study is supported by contracts HHSN268201300025C, HHSN268201300026C, HHSN268201300028C, HHSN268201300029C, and HHSN268200900041C from the National Heart, Lung, and Blood Institute (NHLBI); the Intramural Research Program of the National Institute on Aging (NIA); and an intra‐agency agreement between the NIA and NHLBI (AG0005) and grant R01HL122477 (to Kalhan). This manuscript has been reviewed by CARDIA for scientific content.
Keywords
- CARDIA
- gene expression
- lung function
- oxidative stress
ASJC Scopus subject areas
- Genetics(clinical)
- Genetics
- Molecular Biology