Abstract
Background Impaired lung function is common and associated with increased risk of cardiovascular disease in epidemiological studies. Increased levels of several inflammatory and cardiovascular disease-related plasma proteins have been associated with impaired lung function. The aim was to study the association between plasma proteomics and forced expiratory volume in 1 s (FEV1), forced vital capacity (FVC) and FEV1/FVC ratio.
Methods We used a discovery and replication approach in two community-based cohorts, EpiHealth and the Malmö Offspring Study (total n=2874), to cross-sectionally study 242 cardiovascular disease- and metabolism-linked proteins in relation to FEV1, FVC (both %predicted) and FEV1/FVC ratio. A false discovery rate of 5% was used as the significance threshold in the discovery cohort.
Results Plasma fatty acid-binding protein 4, interleukin-1 receptor antagonist, interleukin-6 and leptin were negatively associated with FEV1 and paraoxonase 3 was positively associated therewith. Fatty acid-binding protein 4, fibroblast growth factor 21, interleukin-1 receptor antagonist, interleukin-6 and leptin were negatively associated with FVC and agouti-related protein, insulin-like growth factor-binding protein 2, paraoxonase 3 and receptor for advanced glycation end products were positively associated therewith. No proteins were associated with FEV1/FVC ratio. A sensitivity analysis in EpiHealth revealed only minor changes after excluding individuals with known cardiovascular disease, diabetes, or obesity.
Conclusions Five proteins were associated with both FEV1 and FVC. Four proteins associated with only FVC and none with FEV1/FVC ratio, suggesting associations mainly through lung volume, not airway obstruction. However, additional studies are needed to investigate underlying mechanisms for these findings.
Footnotes
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Conflicts of interest: A. Rydell has received lecturing fees from AstraZeneca.
Conflicts of interest: Karin Lisspers has received lecturing fees from AstraZeneca, Novartis and Boehringer Ingelheim; and payments for advisory board membership from AstraZeneca, Boehringer Ingelheim and GlaxoSmithKline.
Conflicts of interest: S. Zaigham has received a research grant from Magnus Bergvalls Stiftelse.
Conflicts of interest: P.M. Nilsson has received lecturing fees from Novartis, Novo Nordisk, Amgen and Boehringer Ingelheim.
Conflicts of interest: J. Ärnlöv has received lecturing fees from AstraZeneca and Novartis and served on advisory boards for AstraZeneca and Boehringer Ingelheim on subjects unrelated to this study.
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- Received June 30, 2022.
- Accepted December 4, 2022.
- Copyright ©The authors 2023
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