Circulating Soluble CD163, Associations With Cardiovascular Outcomes and Mortality, and Identification of Genetic Variants in Older Individuals: The Cardiovascular Health Study

Background Monocytes/macrophages participate in cardiovascular disease. CD163 (cluster of differentiation 163) is a monocyte/macrophage receptor, and the shed sCD163 (soluble CD163) reflects monocyte/macrophage activation. We examined the association of sCD163 with incident cardiovascular disease ev...

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Vydané v:Journal of the American Heart Association Ročník 11; číslo 21; s. e024374
Hlavní autori: Durda, Peter, Raffield, Laura M., Lange, Ethan M., Olson, Nels C., Jenny, Nancy Swords, Cushman, Mary, Deichgraeber, Pia, Grarup, Niels, Jonsson, Anna, Hansen, Torben, Mychaleckyj, Josyf C., Psaty, Bruce M., Reiner, Alex P., Tracy, Russell P., Lange, Leslie A.
Médium: Journal Article
Jazyk:English
Vydavateľské údaje: England John Wiley and Sons Inc 01.11.2022
Wiley
Predmet:
Aged
Antigens, CD - blood
Antigens, Differentiation, Myelomonocytic - genetics
Asialoglycoprotein Receptor
Biomarkers
cardiovascular diseases
Cardiovascular Diseases - diagnosis
Cardiovascular Diseases - epidemiology
Cardiovascular Diseases - genetics
CD163 Antigen
Female
Genome-Wide Association Study
Heart Failure
Humans
Longitudinal Studies
Male
monocytes
Original Research
risk factors
CD163 antigen
monocytes
risk factors
cardiovascular diseases
genome‐wide association study
humans
ISSN:2047-9980, 2047-9980
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Abstract Background Monocytes/macrophages participate in cardiovascular disease. CD163 (cluster of differentiation 163) is a monocyte/macrophage receptor, and the shed sCD163 (soluble CD163) reflects monocyte/macrophage activation. We examined the association of sCD163 with incident cardiovascular disease events and performed a genome-wide association study to identify sCD163-associated variants. Methods and Results We measured plasma sCD163 in 5214 adults (aged ≥65 years, 58.7% women, 16.2% Black) of the CHS (Cardiovascular Health Study). We used Cox regression models (associations of sCD163 with incident events and mortality); median follow-up was 26 years. Genome-wide association study analyses were stratified on race. Adjusted for age, sex, and race and ethnicity, sCD163 levels were associated with all-cause mortality (hazard ratio [HR], 1.08 [95% CI, 1.04-1.12] per SD increase), cardiovascular disease mortality (HR, 1.15 [95% CI, 1.09-1.21]), incident coronary heart disease (HR, 1.10 [95% CI, 1.04-1.16]), and incident heart failure (HR, 1.18 [95% CI, 1.12-1.25]). When further adjusted (eg, cardiovascular disease risk factors), only incident coronary heart disease lost significance. In European American individuals, genome-wide association studies identified 38 variants on chromosome 2 near (top result rs62165726, =3.3×10 ),19 variants near chromosome 17 gene (rs55714927, =1.5×10 ), and 18 variants near chromosome 11 gene . These regions replicated in the European ancestry ADDITION-PRO cohort, a longitudinal cohort study nested in the Danish arm of the Anglo-Danish-Dutch study of Intensive Treatment Intensive Treatment In peOple with screeNdetcted Diabetes in Primary Care. In Black individuals, we identified 9 variants on chromosome 6 (rs3129781 =7.1×10 ) in the region, and 3 variants (rs115391969 =4.3×10 ) near the chromosome 16 gene Conclusions Monocyte function, as measured by sCD163, may be predictive of overall and cardiovascular-specific mortality and incident heart failure.
AbstractList Background Monocytes/macrophages participate in cardiovascular disease. CD163 (cluster of differentiation 163) is a monocyte/macrophage receptor, and the shed sCD163 (soluble CD163) reflects monocyte/macrophage activation. We examined the association of sCD163 with incident cardiovascular disease events and performed a genome‐wide association study to identify sCD163‐associated variants. Methods and Results We measured plasma sCD163 in 5214 adults (aged ≥65 years, 58.7% women, 16.2% Black) of the CHS (Cardiovascular Health Study). We used Cox regression models (associations of sCD163 with incident events and mortality); median follow‐up was 26 years. Genome‐wide association study analyses were stratified on race. Adjusted for age, sex, and race and ethnicity, sCD163 levels were associated with all‐cause mortality (hazard ratio [HR], 1.08 [95% CI, 1.04–1.12] per SD increase), cardiovascular disease mortality (HR, 1.15 [95% CI, 1.09–1.21]), incident coronary heart disease (HR, 1.10 [95% CI, 1.04–1.16]), and incident heart failure (HR, 1.18 [95% CI, 1.12–1.25]). When further adjusted (eg, cardiovascular disease risk factors), only incident coronary heart disease lost significance. In European American individuals, genome‐wide association studies identified 38 variants on chromosome 2 near MGAT5 (top result rs62165726, P=3.3×10−18),19 variants near chromosome 17 gene ASGR1 (rs55714927, P=1.5×10−14), and 18 variants near chromosome 11 gene ST3GAL4. These regions replicated in the European ancestry ADDITION‐PRO cohort, a longitudinal cohort study nested in the Danish arm of the Anglo‐Danish‐Dutch study of Intensive Treatment Intensive Treatment In peOple with screeNdetcted Diabetes in Primary Care. In Black individuals, we identified 9 variants on chromosome 6 (rs3129781 P=7.1×10−9) in the HLA region, and 3 variants (rs115391969 P=4.3×10−8) near the chromosome 16 gene MYLK3. Conclusions Monocyte function, as measured by sCD163, may be predictive of overall and cardiovascular‐specific mortality and incident heart failure.
Background Monocytes/macrophages participate in cardiovascular disease. CD163 (cluster of differentiation 163) is a monocyte/macrophage receptor, and the shed sCD163 (soluble CD163) reflects monocyte/macrophage activation. We examined the association of sCD163 with incident cardiovascular disease events and performed a genome-wide association study to identify sCD163-associated variants. Methods and Results We measured plasma sCD163 in 5214 adults (aged ≥65 years, 58.7% women, 16.2% Black) of the CHS (Cardiovascular Health Study). We used Cox regression models (associations of sCD163 with incident events and mortality); median follow-up was 26 years. Genome-wide association study analyses were stratified on race. Adjusted for age, sex, and race and ethnicity, sCD163 levels were associated with all-cause mortality (hazard ratio [HR], 1.08 [95% CI, 1.04-1.12] per SD increase), cardiovascular disease mortality (HR, 1.15 [95% CI, 1.09-1.21]), incident coronary heart disease (HR, 1.10 [95% CI, 1.04-1.16]), and incident heart failure (HR, 1.18 [95% CI, 1.12-1.25]). When further adjusted (eg, cardiovascular disease risk factors), only incident coronary heart disease lost significance. In European American individuals, genome-wide association studies identified 38 variants on chromosome 2 near MGAT5 (top result rs62165726, P=3.3×10-18),19 variants near chromosome 17 gene ASGR1 (rs55714927, P=1.5×10-14), and 18 variants near chromosome 11 gene ST3GAL4. These regions replicated in the European ancestry ADDITION-PRO cohort, a longitudinal cohort study nested in the Danish arm of the Anglo-Danish-Dutch study of Intensive Treatment Intensive Treatment In peOple with screeNdetcted Diabetes in Primary Care. In Black individuals, we identified 9 variants on chromosome 6 (rs3129781 P=7.1×10-9) in the HLA region, and 3 variants (rs115391969 P=4.3×10-8) near the chromosome 16 gene MYLK3. Conclusions Monocyte function, as measured by sCD163, may be predictive of overall and cardiovascular-specific mortality and incident heart failure.Background Monocytes/macrophages participate in cardiovascular disease. CD163 (cluster of differentiation 163) is a monocyte/macrophage receptor, and the shed sCD163 (soluble CD163) reflects monocyte/macrophage activation. We examined the association of sCD163 with incident cardiovascular disease events and performed a genome-wide association study to identify sCD163-associated variants. Methods and Results We measured plasma sCD163 in 5214 adults (aged ≥65 years, 58.7% women, 16.2% Black) of the CHS (Cardiovascular Health Study). We used Cox regression models (associations of sCD163 with incident events and mortality); median follow-up was 26 years. Genome-wide association study analyses were stratified on race. Adjusted for age, sex, and race and ethnicity, sCD163 levels were associated with all-cause mortality (hazard ratio [HR], 1.08 [95% CI, 1.04-1.12] per SD increase), cardiovascular disease mortality (HR, 1.15 [95% CI, 1.09-1.21]), incident coronary heart disease (HR, 1.10 [95% CI, 1.04-1.16]), and incident heart failure (HR, 1.18 [95% CI, 1.12-1.25]). When further adjusted (eg, cardiovascular disease risk factors), only incident coronary heart disease lost significance. In European American individuals, genome-wide association studies identified 38 variants on chromosome 2 near MGAT5 (top result rs62165726, P=3.3×10-18),19 variants near chromosome 17 gene ASGR1 (rs55714927, P=1.5×10-14), and 18 variants near chromosome 11 gene ST3GAL4. These regions replicated in the European ancestry ADDITION-PRO cohort, a longitudinal cohort study nested in the Danish arm of the Anglo-Danish-Dutch study of Intensive Treatment Intensive Treatment In peOple with screeNdetcted Diabetes in Primary Care. In Black individuals, we identified 9 variants on chromosome 6 (rs3129781 P=7.1×10-9) in the HLA region, and 3 variants (rs115391969 P=4.3×10-8) near the chromosome 16 gene MYLK3. Conclusions Monocyte function, as measured by sCD163, may be predictive of overall and cardiovascular-specific mortality and incident heart failure.
Background Monocytes/macrophages participate in cardiovascular disease. CD163 (cluster of differentiation 163) is a monocyte/macrophage receptor, and the shed sCD163 (soluble CD163) reflects monocyte/macrophage activation. We examined the association of sCD163 with incident cardiovascular disease events and performed a genome-wide association study to identify sCD163-associated variants. Methods and Results We measured plasma sCD163 in 5214 adults (aged ≥65 years, 58.7% women, 16.2% Black) of the CHS (Cardiovascular Health Study). We used Cox regression models (associations of sCD163 with incident events and mortality); median follow-up was 26 years. Genome-wide association study analyses were stratified on race. Adjusted for age, sex, and race and ethnicity, sCD163 levels were associated with all-cause mortality (hazard ratio [HR], 1.08 [95% CI, 1.04-1.12] per SD increase), cardiovascular disease mortality (HR, 1.15 [95% CI, 1.09-1.21]), incident coronary heart disease (HR, 1.10 [95% CI, 1.04-1.16]), and incident heart failure (HR, 1.18 [95% CI, 1.12-1.25]). When further adjusted (eg, cardiovascular disease risk factors), only incident coronary heart disease lost significance. In European American individuals, genome-wide association studies identified 38 variants on chromosome 2 near (top result rs62165726, =3.3×10 ),19 variants near chromosome 17 gene (rs55714927, =1.5×10 ), and 18 variants near chromosome 11 gene . These regions replicated in the European ancestry ADDITION-PRO cohort, a longitudinal cohort study nested in the Danish arm of the Anglo-Danish-Dutch study of Intensive Treatment Intensive Treatment In peOple with screeNdetcted Diabetes in Primary Care. In Black individuals, we identified 9 variants on chromosome 6 (rs3129781 =7.1×10 ) in the region, and 3 variants (rs115391969 =4.3×10 ) near the chromosome 16 gene Conclusions Monocyte function, as measured by sCD163, may be predictive of overall and cardiovascular-specific mortality and incident heart failure.
Author Durda, Peter
Jenny, Nancy Swords
Grarup, Niels
Lange, Ethan M.
Olson, Nels C.
Psaty, Bruce M.
Lange, Leslie A.
Tracy, Russell P.
Cushman, Mary
Jonsson, Anna
Hansen, Torben
Mychaleckyj, Josyf C.
Raffield, Laura M.
Deichgraeber, Pia
Reiner, Alex P.
AuthorAffiliation 3 Department of Biochemistry Larner College of Medicine, University of Vermont Burlington VT
6 Steno Diabetes Center Aarhus University Hospital Aarhus Denmark
11 Department of Epidemiology University of Washington Seattle WA
10 Cardiovascular Health Research Unit, Departments of Medicine, Epidemiology and Health Services University of Washington Seattle WA
8 Novo Nordisk Foundation Center for Basic Metabolic Research Copenhagen Denmark
1 Department of Pathology and Laboratory Medicine Larner College of Medicine, University of Vermont Burlington VT
2 Department of Medicine Larner College of Medicine, University of Vermont Burlington VT
7 Department of Endocrinology and Internal Medicine Aarhus University Hospital Aarhus Denmark
5 Division of Biomedical Informatics and Personalized Medicine, Department of Medicine University of Colorado Anschutz Medical Campus Aurora CO
4 Department of Genetics University of North Carolina Chapel Hill NC
9 Center for Public Health Genomics University of Virginia C
AuthorAffiliation_xml – name: 7 Department of Endocrinology and Internal Medicine Aarhus University Hospital Aarhus Denmark
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Issue 21
Keywords CD163 antigen
monocytes
risk factors
cardiovascular diseases
genome‐wide association study
humans
Language English
License This is an open access article under the terms of the http://creativecommons.org/licenses/by-nc-nd/4.0/ License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non‐commercial and no modifications or adaptations are made.
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content type line 23
R. P. Tracy and L. A. Lange contributed equally.
For Sources of Funding and Disclosures, see page 12.
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PublicationTitle Journal of the American Heart Association
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Snippet Background Monocytes/macrophages participate in cardiovascular disease. CD163 (cluster of differentiation 163) is a monocyte/macrophage receptor, and the shed...
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SubjectTerms Aged
Antigens, CD - blood
Antigens, Differentiation, Myelomonocytic - genetics
Asialoglycoprotein Receptor
Biomarkers
cardiovascular diseases
Cardiovascular Diseases - diagnosis
Cardiovascular Diseases - epidemiology
Cardiovascular Diseases - genetics
CD163 Antigen
Female
Genome-Wide Association Study
Heart Failure
Humans
Longitudinal Studies
Male
monocytes
Original Research
risk factors
Title Circulating Soluble CD163, Associations With Cardiovascular Outcomes and Mortality, and Identification of Genetic Variants in Older Individuals: The Cardiovascular Health Study
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