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Publications (10 of 289) Show all publications
Suzuki, K., Giedraitis, V., Ingelsson, M., Lind, L., Ingelsson, E. & Zeggini, E. (2024). Genetic drivers of heterogeneity in type 2 diabetes pathophysiology. Nature, 627(8003), 347-357
Open this publication in new window or tab >>Genetic drivers of heterogeneity in type 2 diabetes pathophysiology
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2024 (English)In: Nature, ISSN 0028-0836, E-ISSN 1476-4687, Vol. 627, no 8003, p. 347-357Article in journal (Refereed) Published
Abstract [en]

Type 2 diabetes (T2D) is a heterogeneous disease that develops through diverse pathophysiological processes1,2 and molecular mechanisms that are often specific to cell type3,4. Here, to characterize the genetic contribution to these processes across ancestry groups, we aggregate genome-wide association study data from 2,535,601 individuals (39.7% not of European ancestry), including 428,452 cases of T2D. We identify 1,289 independent association signals at genome-wide significance (P < 5 × 10−8) that map to 611 loci, of which 145 loci are, to our knowledge, previously unreported. We define eight non-overlapping clusters of T2D signals that are characterized by distinct profiles of cardiometabolic trait associations. These clusters are differentially enriched for cell-type-specific regions of open chromatin, including pancreatic islets, adipocytes, endothelial cells and enteroendocrine cells. We build cluster-specific partitioned polygenic scores5 in a further 279,552 individuals of diverse ancestry, including 30,288 cases of T2D, and test their association with T2D-related vascular outcomes. Cluster-specific partitioned polygenic scores are associated with coronary artery disease, peripheral artery disease and end-stage diabetic nephropathy across ancestry groups, highlighting the importance of obesity-related processes in the development of vascular outcomes. Our findings show the value of integrating multi-ancestry genome-wide association study data with single-cell epigenomics to disentangle the aetiological heterogeneity that drives the development and progression of T2D. This might offer a route to optimize global access to genetically informed diabetes care.

Place, publisher, year, edition, pages
Springer Nature, 2024
National Category
Endocrinology and Diabetes Medical Genetics and Genomics
Identifiers
urn:nbn:se:uu:diva-533526 (URN)10.1038/s41586-024-07019-6 (DOI)001185035100001 ()38374256 (PubMedID)
Funder
EU, Horizon 2020, 101017802
Note

For complete list of authors see http://dx.doi.org/10.1038/s41586-024-07019-6

Available from: 2024-06-27 Created: 2024-06-27 Last updated: 2025-02-10Bibliographically approved
Gustafsson, S., Lampa, E., Jensevik Eriksson, K., Butterworth, A. S., Elmståhl, S., Engström, G., . . . Sundström, J. (2024). Markers of imminent myocardial infarction. Nature Cardiovascular Research, 3(2), 130-139
Open this publication in new window or tab >>Markers of imminent myocardial infarction
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2024 (English)In: Nature Cardiovascular Research, E-ISSN 2731-0590, Vol. 3, no 2, p. 130-139Article in journal (Refereed) Published
Abstract [en]

Myocardial infarction is a leading cause of death globally but is notoriously difficult to predict. We aimed to identify biomarkers of an imminent first myocardial infarction and design relevant prediction models. Here, we constructed a new case–cohort consortium of 2,018 persons without prior cardiovascular disease from six European cohorts, among whom 420 developed a first myocardial infarction within 6 months after the baseline blood draw. We analyzed 817 proteins and 1,025 metabolites in biobanked blood and 16 clinical variables. Forty-eight proteins, 43 metabolites, age, sex and systolic blood pressure were associated with the risk of an imminent first myocardial infarction. Brain natriuretic peptide was most consistently associated with the risk of imminent myocardial infarction. Using clinically readily available variables, we devised a prediction model for an imminent first myocardial infarction for clinical use in the general population, with good discriminatory performance and potential for motivating primary prevention efforts.

Place, publisher, year, edition, pages
Springer Nature, 2024
National Category
Cardiology and Cardiovascular Disease
Identifiers
urn:nbn:se:uu:diva-523069 (URN)10.1038/s44161-024-00422-2 (DOI)001160066800002 ()39196201 (PubMedID)
Funder
Uppsala UniversityEU, FP7, Seventh Framework Programme, 313010European Regional Development Fund (ERDF), 2014-2020.4.01.15-0012European Commission, HEALTH-F2-2012-279233EU, European Research Council, 268834Swedish Cancer SocietySwedish Research Council, 2019-01471Region SkåneRegion VästerbottenSwedish Heart Lung Foundation, 20190505Knut and Alice Wallenberg FoundationVinnovaEU, European Research Council, 801965AFA Insurance, 160266Swedish Research Council, 2016-01065Swedish Heart Lung Foundation, 20160734Swedish National Infrastructure for Computing (SNIC), sens2019006Swedish National Infrastructure for Computing (SNIC), sens2020005UPPMAXSwedish Research Council, 2018-05973
Note

These authors contributed equally: Stefan Gustafsson, Erik Lampa

Available from: 2024-02-13 Created: 2024-02-13 Last updated: 2025-02-10Bibliographically approved
Ganji-Arjenaki, M., Kamali, Z., Sardari, S., de Borst, M., Snieder, H. & Vaez, A. (2024). Prioritization of Kidney Cell Types Highlights Myofibroblast Cells in Regulating Human Blood Pressure. Kidney international reports, 9(6), 1849-1859
Open this publication in new window or tab >>Prioritization of Kidney Cell Types Highlights Myofibroblast Cells in Regulating Human Blood Pressure
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2024 (English)In: Kidney international reports, ISSN 2468-0249, Vol. 9, no 6, p. 1849-1859Article in journal (Refereed) Published
Abstract [en]

INTRODUCTION: Blood pressure (BP) is a highly heritable trait with over 2000 underlying genomic loci identified to date. Although the kidney plays a key role, little is known about specific cell types involved in the genetic regulation of BP.

METHODS: Here, we applied stratified linkage disequilibrium score (LDSC) regression to connect BP genome-wide association studies (GWAS) results to specific cell types of the mature human kidney. We used the largest single-stage BP genome-wide analysis to date, including up to 1,028,980 adults of European ancestry, and single-cell transcriptomic data from 14 mature human kidneys, with mean age of 41 years.

RESULTS: Our analyses prioritized myofibroblasts and endothelial cells, among the total of 33 annotated cell type, as specifically involved in BP regulation (P < 0.05/33, i.e., 0.001515). Enrichment of heritability for systolic BP (SBP) was observed in myofibroblast cells in mature human kidney cortex, and enrichment of heritability for diastolic BP (DBP) was observed in descending vasa recta and peritubular capillary endothelial cells as well as stromal myofibroblast cells. The new finding of myofibroblast, the significant cell type for both BP traits, was consistent in 8 replication efforts using 7 sets of independent data, including in human fetal kidney, in East-Asian (EAS) ancestry, using mouse single-cell RNA sequencing (scRNA-seq) data, and when using another prioritization method.

CONCLUSION: Our findings provide a solid basis for follow-up studies to further identify genes and mechanisms in myofibroblast cells that underlie the regulation of BP.

Place, publisher, year, edition, pages
Elsevier, 2024
Keywords
blood pressure, cell-type, genome, kidney myofibroblast, scRNA-seq
National Category
Cell and Molecular Biology
Identifiers
urn:nbn:se:uu:diva-548845 (URN)10.1016/j.ekir.2024.03.001 (DOI)001251948600001 ()38899223 (PubMedID)2-s2.0-85190342984 (Scopus ID)
Note

Stefan Enroth, Vilmantas Giedraitis, Ulf Gyllensten, Erik Ingelsson, Åsa Johansson, Lars Lind, Johan Sundström are members in the International Consortium of Blood Pressure

For complete list of contributors see https://doi.org/10.1016/j.ekir.2024.03.001

Available from: 2025-01-29 Created: 2025-01-29 Last updated: 2025-01-29Bibliographically approved
Tängdén, T., Gustafsson, S., Rao, A. S. & Ingelsson, E. (2022). A genome-wide association study in a large community-based cohort identifies multiple loci associated with susceptibility to bacterial and viral infections. Scientific Reports, 12, Article ID 2582.
Open this publication in new window or tab >>A genome-wide association study in a large community-based cohort identifies multiple loci associated with susceptibility to bacterial and viral infections
2022 (English)In: Scientific Reports, E-ISSN 2045-2322, Vol. 12, article id 2582Article in journal (Refereed) Published
Abstract [en]

There is limited data on host-specific genetic determinants of susceptibility to bacterial and viral infections. Genome-wide association studies using large population cohorts can be a first step towards identifying patients prone to infectious diseases and targets for new therapies. Genetic variants associated with clinically relevant entities of bacterial and viral infections (e.g., abdominal infections, respiratory infections, and sepsis) in 337,484 participants of the UK Biobank cohort were explored by genome-wide association analyses. Cases (n = 81,179) were identified based on ICD-10 diagnosis codes of hospital inpatient and death registries. Functional annotation was performed using gene expression (eQTL) data. Fifty-seven unique genome-wide significant loci were found, many of which are novel in the context of infectious diseases. Some of the detected genetic variants were previously reported associated with infectious, inflammatory, autoimmune, and malignant diseases or key components of the immune system (e.g., white blood cells, cytokines). Fine mapping of the HLA region revealed significant associations with HLA-DQA1, HLA-DRB1, and HLA-DRB4 locus alleles. PPP1R14A showed strong colocalization with abdominal infections and gene expression in sigmoid and transverse colon, suggesting causality. Shared significant loci across infections and non-infectious phenotypes in the UK Biobank cohort were found, suggesting associations for example between SNPs identified for abdominal infections and CRP, rheumatoid arthritis, and diabetes mellitus. We report multiple loci associated with bacterial and viral infections. A better understanding of the genetic determinants of bacterial and viral infections can be useful to identify patients at risk and in the development of new drugs.

Place, publisher, year, edition, pages
Springer NatureSpringer Nature, 2022
National Category
Infectious Medicine
Identifiers
urn:nbn:se:uu:diva-470538 (URN)10.1038/s41598-022-05838-z (DOI)000757107700002 ()35173190 (PubMedID)
Funder
Swedish Research Council, 2019-05911Swedish Research Council, 2020-02320Knut and Alice Wallenberg Foundation, 2013.0126
Available from: 2022-03-29 Created: 2022-03-29 Last updated: 2024-01-15Bibliographically approved
Ramdas, S., Gustafsson, S., Lind, L., Ingelsson, E. & Brown, C. D. (2022). A multi-layer functional genomic analysis to understand noncoding genetic variation in lipids. American Journal of Human Genetics, 109(8), 1366-1387
Open this publication in new window or tab >>A multi-layer functional genomic analysis to understand noncoding genetic variation in lipids
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2022 (English)In: American Journal of Human Genetics, ISSN 0002-9297, E-ISSN 1537-6605, Vol. 109, no 8, p. 1366-1387Article in journal (Refereed) Published
Abstract [en]

A major challenge of genome-wide association studies (GWASs) is to translate phenotypic associations into biological insights. Here, we integrate a large GWAS on blood lipids involving 1.6 million individuals from five ancestries with a wide array of functional genomic datasets to discover regulatory mechanisms underlying lipid associations. We first prioritize lipid-associated genes with expression quantitative trait locus (eQTL) colocalizations and then add chromatin interaction data to narrow the search for functional genes. Polygenic enrichment analysis across 697 annotations from a host of tissues and cell types confirms the central role of the liver in lipid levels and highlights the selective enrichment of adipose-specific chromatin marks in high-density lipoprotein cholesterol and triglycerides. Overlapping transcription factor (TF) binding sites with lipid-associated loci identifies TFs relevant in lipid biology. In addition, we present an integrative framework to prioritize causal variants at GWAS loci, producing a comprehensive list of candidate causal genes and variants with multiple layers of functional evidence. We highlight two of the prioritized genes, CREBRF and RRBP1, which show convergent evidence across functional datasets supporting their roles in lipid biology.

Place, publisher, year, edition, pages
Cell PressCELL PRESS, 2022
National Category
Medical Genetics and Genomics
Identifiers
urn:nbn:se:uu:diva-485348 (URN)10.1016/j.ajhg.2022.06.012 (DOI)000850681500003 ()35931049 (PubMedID)
Note

For complete list of authors see http://dx.doi.org/10.1016/j.ajhg.2022.06.012

De fem första författarna delar förstaförfattarskapet.

Available from: 2022-09-22 Created: 2022-09-22 Last updated: 2025-02-10Bibliographically approved
Kanoni, S., Gustafsson, S., Lind, L., Ingelsson, E. & Demirkan, A. (2022). Implicating genes, pleiotropy, and sexual dimorphism at blood lipid loci through multi-ancestry meta-analysis. Genome Biology, 23, Article ID 268.
Open this publication in new window or tab >>Implicating genes, pleiotropy, and sexual dimorphism at blood lipid loci through multi-ancestry meta-analysis
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2022 (English)In: Genome Biology, ISSN 1465-6906, E-ISSN 1474-760X, Vol. 23, article id 268Article in journal (Refereed) Published
Abstract [en]

Background: Genetic variants within nearly 1000 loci are known to contribute to modulation of blood lipid levels. However, the biological pathways underlying these associations are frequently unknown, limiting understanding of these findings and hindering downstream translational efforts such as drug target discovery.

Results: To expand our understanding of the underlying biological pathways and mechanisms controlling blood lipid levels, we leverage a large multi-ancestry meta-analysis (N=1,654,960) of blood lipids to prioritize putative causal genes for 2286 lipid associations using six gene prediction approaches. Using phenome-wide association (PheWAS) scans, we identify relationships of genetically predicted lipid levels to other diseases and conditions. We confirm known pleiotropic associations with cardiovascular phenotypes and determine novel associations, notably with cholelithiasis risk. We perform sex-stratified GWAS meta-analysis of lipid levels and show that 3-5% of autosomal lipid-associated loci demonstrate sex-biased effects. Finally, we report 21 novel lipid loci identified on the X chromosome. Many of the sex-biased autosomal and X chromosome lipid loci show pleiotropic associations with sex hormones, emphasizing the role of hormone regulation in lipid metabolism.

Conclusions: Taken together, our findings provide insights into the biological mechanisms through which associated variants lead to altered lipid levels and potentially cardiovascular disease risk.

Place, publisher, year, edition, pages
BioMed Central (BMC), 2022
Keywords
Cholesterol, Lipids, Genetics, Genome-wide association study, GWAS
National Category
Medical Genetics and Genomics
Identifiers
urn:nbn:se:uu:diva-498949 (URN)10.1186/s13059-022-02837-1 (DOI)000927879600003 ()36575460 (PubMedID)
Funder
Wellcome trust, 201543/B/16/ZWellcome trust, 202802/Z/16/ZEU, FP7, Seventh Framework Programme, HEALTH-F2-2013-601456EU, FP7, Seventh Framework Programme, 608765EU, FP7, Seventh Framework Programme, 786833Novo Nordisk, NNF15CC0018486Academy of Finland, 312062
Note

For complete list of authors see http://dx.doi.org/10.1186/s13059-022-02837-1

Available from: 2023-03-22 Created: 2023-03-22 Last updated: 2025-02-10Bibliographically approved
Mahajan, A., Spracklen, C. N., Zhang, W., Ng, M. C. Y., Petty, L. E., Kitajima, H., . . . Morris, A. P. (2022). Multi-ancestry genetic study of type 2 diabetes highlights the power of diverse populations for discovery and translation. Nature Genetics, 54(5), 560-572
Open this publication in new window or tab >>Multi-ancestry genetic study of type 2 diabetes highlights the power of diverse populations for discovery and translation
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2022 (English)In: Nature Genetics, ISSN 1061-4036, E-ISSN 1546-1718, Vol. 54, no 5, p. 560-572Article in journal (Refereed) Published
Abstract [en]

We assembled an ancestrally diverse collection of genome-wide association studies (GWAS) of type 2 diabetes (T2D) in 180,834 affected individuals and 1,159,055 controls (48.9% non-European descent) through the Diabetes Meta-Analysis of Trans-Ethnic association studies (DIAMANTE) Consortium. Multi-ancestry GWAS meta-analysis identified 237 loci attaining stringent genome-wide significance (P < 5 x 10(-9)), which were delineated to 338 distinct association signals. Fine-mapping of these signals was enhanced by the increased sample size and expanded population diversity of the multi-ancestry meta-analysis, which localized 54.4% of T2D associations to a single variant with >50% posterior probability. This improved fine-mapping enabled systematic assessment of candidate causal genes and molecular mechanisms through which T2D associations are mediated, laying the foundations for functional investigations. Multi-ancestry genetic risk scores enhanced transferability of T2D prediction across diverse populations. Our study provides a step toward more effective clinical translation of T2D GWAS to improve global health for all, irrespective of genetic background. Genome-wide association and fine-mapping analyses in ancestrally diverse populations implicate candidate causal genes and mechanisms underlying type 2 diabetes. Trans-ancestry genetic risk scores enhance transferability across populations.

Place, publisher, year, edition, pages
Springer NatureSpringer Nature, 2022
National Category
Medical Genetics and Genomics
Identifiers
urn:nbn:se:uu:diva-476118 (URN)10.1038/s41588-022-01058-3 (DOI)000794118000004 ()35551307 (PubMedID)
Available from: 2022-06-07 Created: 2022-06-07 Last updated: 2025-02-10Bibliographically approved
Mishra, A., den Hoed, M., Gustafsson, S., Ingelsson, E., Ingelsson, M., Lind, L. & Gravel, S. (2022). Stroke genetics informs drug discovery and risk prediction across ancestries. Nature, 611(7934), 115-+
Open this publication in new window or tab >>Stroke genetics informs drug discovery and risk prediction across ancestries
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2022 (English)In: Nature, ISSN 0028-0836, E-ISSN 1476-4687, Vol. 611, no 7934, p. 115-+Article in journal (Refereed) Published
Abstract [en]

Previous genome-wide association studies (GWASs) of stroke - the second leading cause of death worldwide - were conducted predominantly in populations of European ancestry(1,2). Here, in cross-ancestry GWAS meta-analyses of 110,182 patients who have had a stroke (five ancestries, 33% non-European) and 1,503,898 control individuals, we identify association signals for stroke and its subtypes at 89 (61 new) independent loci: 60 in primary inverse-variance-weighted analyses and 29 in secondary meta-regression and multitrait analyses. On the basis of internal cross-ancestry validation and an independent follow-up in 89,084 additional cases of stroke (30% non-European) and 1,013,843 control individuals, 87% of the primary stroke risk loci and 60% of the secondary stroke risk loci were replicated (P < 0.05). Effect sizes were highly correlated across ancestries. Cross-ancestry fine-mapping, in silico mutagenesis analysis(3), and transcriptome-wide and proteome-wide association analyses revealed putative causal genes (such as SH3PXD2A and FURIN) and variants (such as at GRK5 and NOS3). Using a three-pronged approach(4), we provide genetic evidence for putative drug effects, highlighting F11, KLKB1, PROC, GP1BA, LAMC2 and VCAM1 as possible targets, with drugs already under investigation for stroke for F11 and PROC. A polygenic score integrating cross-ancestry and ancestry-specific stroke GWASs with vascular-risk factor GWASs (integrative polygenic scores) strongly predicted ischaemic stroke in populations of European, East Asian and African ancestry(5). Stroke genetic risk scores were predictive of ischaemic stroke independent of clinical risk factors in 52,600 clinical-trial participants with cardiometabolic disease. Our results provide insights to inform biology, reveal potential drug targets and derive genetic risk prediction tools across ancestries.

Place, publisher, year, edition, pages
Springer Nature, 2022
National Category
Medical Genetics and Genomics Neurology
Identifiers
urn:nbn:se:uu:diva-540306 (URN)10.1038/s41586-022-05165-3 (DOI)000862209300001 ()36180795 (PubMedID)
Note

For complete list of authors see http://dx.doi.org/10.1038/s41586-022-05165-3

Correction in: Nature, volume 612, page E7 (2022)

DOI: 10.1038/s41586-022-05492-5

Available from: 2024-10-14 Created: 2024-10-14 Last updated: 2025-02-10Bibliographically approved
Jhun, M.-A., Mendelson, M., Wilson, R., Gondalia, R., Joehanes, R., Salfati, E., . . . Assimes, T. L. (2021). A multi-ethnic epigenome-wide association study of leukocyte DNA methylation and blood lipids. Nature Communications, 12(1), Article ID 3987.
Open this publication in new window or tab >>A multi-ethnic epigenome-wide association study of leukocyte DNA methylation and blood lipids
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2021 (English)In: Nature Communications, E-ISSN 2041-1723, Vol. 12, no 1, article id 3987Article in journal (Refereed) Published
Abstract [en]

Here we examine the association between DNA methylation in circulating leukocytes and blood lipids in a multi-ethnic sample of 16,265 subjects. We identify 148, 35, and 4 novel associations among Europeans, African Americans, and Hispanics, respectively, and an additional 186 novel associations through a trans-ethnic meta-analysis. We observe a high concordance in the direction of effects across racial/ethnic groups, a high correlation of effect sizes between high-density lipoprotein and triglycerides, a modest overlap of associations with epigenome-wide association studies of other cardio-metabolic traits, and a largely non-overlap with lipid loci identified to date through genome-wide association studies. Thirty CpGs reached significance in at least 2 racial/ethnic groups including 7 that showed association with the expression of an annotated gene. CpGs annotated to CPT1A showed evidence of being influenced by triglycerides levels. DNA methylation levels of circulating leukocytes show robust and consistent association with blood lipid levels across multiple racial/ethnic groups. Abnormal blood lipid levels are important risk factors for cardiovascular and other various diseases. Here the authors conduct a large-scale multi-ethnic epigenome-wide association study combined with epigenetic (cis-QTL and eQTM) data, and identify CpG-lipid traits associations that are specific to or common across racial/ethnic groups.

Place, publisher, year, edition, pages
Springer NatureNATURE RESEARCH, 2021
National Category
Medical Genetics and Genomics
Identifiers
urn:nbn:se:uu:diva-451570 (URN)10.1038/s41467-021-23899-y (DOI)000669943800001 ()34183656 (PubMedID)
Funder
EU, FP7, Seventh Framework ProgrammeSwedish Research Council, 2012-1397Knut and Alice Wallenberg Foundation, 2013.0126Swedish Heart Lung Foundation, 20140422
Available from: 2021-09-16 Created: 2021-09-16 Last updated: 2025-02-10Bibliographically approved
Rydell, A., Nowak, C., Janson, C., Lisspers, K., Ställberg, B., Iggman, D., . . . Ärnlöv, J. (2021). Plasma proteomics and lung function in four community-based cohorts. Respiratory Medicine, 176, Article ID 106282.
Open this publication in new window or tab >>Plasma proteomics and lung function in four community-based cohorts
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2021 (English)In: Respiratory Medicine, ISSN 0954-6111, E-ISSN 1532-3064, Vol. 176, article id 106282Article in journal (Refereed) Published
Abstract [en]

BACKGROUND: Underlying mechanism leading to impaired lung function are incompletely understood.

OBJECTIVES: To investigate whether protein profiling can provide novel insights into mechanisms leading to impaired lung function.

METHODS: We used four community-based studies (n = 2552) to investigate associations between 79 cardiovascular/inflammatory proteins and forced expiratory volume in 1 s percent predicted (FEV1%) assessed by spirometry. We divided the cohorts into discovery and replication samples and used risk factor-adjusted linear regression corrected for multiple comparison (false discovery rate of 5%). We performed Mendelian randomization analyses using genetic and spirometry data from the UK Biobank (n = 421,986) to assess causality.

MEASUREMENTS AND MAIN RESULTS: In cross-sectional analysis, 22 proteins were associated with lower FEV1% in both the discovery and replication sample, regardless of stratification by smoking status. The combined proteomic data cumulatively explained 5% of the variation in FEV1%. In longitudinal analyses (n = 681), higher plasma levels of growth differentiation factor 15 (GDF-15) and interleukin 6 (IL-6) predicted a more rapid 5-year decline in lung function (change in FEV1% per standard deviation of protein level -1.4, (95% CI, -2.5 to -0.3) for GDF-15, and -0.8, (95% CI, -1.5 to -0.2) for IL-6. Mendelian randomization analysis in UK-biobank provided support for a causal effect of increased GDF-15 levels and reduced FEV1%.

CONCLUSIONS: Our combined approach identified GDF-15 as a potential causal factor in the development of impaired lung function in the general population. These findings encourage additional studies evaluating the role of GDF-15 as a causal factor for impaired lung function.

Place, publisher, year, edition, pages
Elsevier, 2021
Keywords
FEV1, Mendelian randomization, Protein expression, Proteomics
National Category
Cardiology and Cardiovascular Disease Respiratory Medicine and Allergy
Identifiers
urn:nbn:se:uu:diva-430538 (URN)10.1016/j.rmed.2020.106282 (DOI)000618529000037 ()33310204 (PubMedID)
Funder
Region DalarnaSwedish Research CouncilSwedish Heart Lung Foundation
Available from: 2021-01-11 Created: 2021-01-11 Last updated: 2025-02-10Bibliographically approved
Organisations
Identifiers
ORCID iD: ORCID iD iconorcid.org/0000-0003-2256-6972

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