Association between cardiovascular disease- and inflammation-related serum biomarkers and poor lung function in elderly.
Cardiovascular disease
Inflammation
Lung function decline
Proteomics
Journal
Clinical proteomics
ISSN: 1542-6416
Titre abrégé: Clin Proteomics
Pays: England
ID NLM: 101184586
Informations de publication
Date de publication:
28 Sep 2021
28 Sep 2021
Historique:
received:
14
06
2021
accepted:
15
09
2021
entrez:
29
9
2021
pubmed:
30
9
2021
medline:
30
9
2021
Statut:
epublish
Résumé
Cardiovascular disease (CVD) is a common comorbidity in chronic obstructive pulmonary disease (COPD) and reduced lung function is an important risk factor for CVD and CVD-related death. However, the mechanisms behind the increased risk for CVD in COPD patients are not fully understood. We examined the association between CVD- and inflammation-related serum biomarkers, and pulmonary function in a geriatric population. 266 biomarkers related to CVD and inflammation were analyzed in blood samples from 611 subjects aged 66-86 years who participated in the Good Aging in Skåne study. Serum levels were assessed by a proximity extension assay. Pulmonary function was measured using the lower limit of normality (LLN) spirometry criteria, i.e., forced expiratory volume in 1 s (FEV1)/forced vital capacity (FVC) < LLN. Logistic regression models were implemented and multiple comparisons were accounted for. 10.3% of the study participants fulfilled pulmonary function decline criteria according to LLN. Out of the 266 biomarkers, only plasminogen activator, urokinase receptor (PLAUR) was statistically significantly associated with decreased pulmonary function. We could not find a statistically significant association between pulmonary function decline and other biomarkers previously linked to COPD, such as interleukin 6, tumor necrosis factor and surfactant protein D. We found that serum levels of PLAUR are associated with pulmonary function decline in older adults. PLAUR is activated following inflammation and promotes matrix metallopeptidase (MMP) activation and extracellular matrix (ECM) degradation. This implies that PLAUR could play a role in the early phase of COPD pathogenesis.
Sections du résumé
BACKGROUND
BACKGROUND
Cardiovascular disease (CVD) is a common comorbidity in chronic obstructive pulmonary disease (COPD) and reduced lung function is an important risk factor for CVD and CVD-related death. However, the mechanisms behind the increased risk for CVD in COPD patients are not fully understood.
METHODS
METHODS
We examined the association between CVD- and inflammation-related serum biomarkers, and pulmonary function in a geriatric population. 266 biomarkers related to CVD and inflammation were analyzed in blood samples from 611 subjects aged 66-86 years who participated in the Good Aging in Skåne study. Serum levels were assessed by a proximity extension assay. Pulmonary function was measured using the lower limit of normality (LLN) spirometry criteria, i.e., forced expiratory volume in 1 s (FEV1)/forced vital capacity (FVC) < LLN. Logistic regression models were implemented and multiple comparisons were accounted for.
RESULTS
RESULTS
10.3% of the study participants fulfilled pulmonary function decline criteria according to LLN. Out of the 266 biomarkers, only plasminogen activator, urokinase receptor (PLAUR) was statistically significantly associated with decreased pulmonary function. We could not find a statistically significant association between pulmonary function decline and other biomarkers previously linked to COPD, such as interleukin 6, tumor necrosis factor and surfactant protein D.
CONCLUSION
CONCLUSIONS
We found that serum levels of PLAUR are associated with pulmonary function decline in older adults. PLAUR is activated following inflammation and promotes matrix metallopeptidase (MMP) activation and extracellular matrix (ECM) degradation. This implies that PLAUR could play a role in the early phase of COPD pathogenesis.
Identifiants
pubmed: 34583636
doi: 10.1186/s12014-021-09329-7
pii: 10.1186/s12014-021-09329-7
pmc: PMC8480099
doi:
Types de publication
Journal Article
Langues
eng
Pagination
23Subventions
Organisme : vetenskapsrådet
ID : 2017-01613
Organisme : vetenskapsrådet
ID : 2017-00639
Informations de copyright
© 2021. The Author(s).
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