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  1. Article: Editorial: Improving Early Detection and Risk Prediction in Heart Failure.

    Tragante, Vinicius / Pilbrow, Anna / Poppe, Katrina

    Frontiers in cardiovascular medicine

    2022  Volume 9, Page(s) 930935

    Language English
    Publishing date 2022-05-18
    Publishing country Switzerland
    Document type Editorial
    ZDB-ID 2781496-8
    ISSN 2297-055X
    ISSN 2297-055X
    DOI 10.3389/fcvm.2022.930935
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  2. Article ; Online: Mendelian randomization: A powerful method to determine causality of biomarkers in diseases.

    Tragante, Vinicius / Asselbergs, Folkert W

    International journal of cardiology

    2018  Volume 268, Page(s) 227–228

    MeSH term(s) Biomarkers ; Causality ; Genetic Variation ; Mendelian Randomization Analysis ; Random Allocation
    Chemical Substances Biomarkers
    Language English
    Publishing date 2018-05-17
    Publishing country Netherlands
    Document type Editorial ; Comment
    ZDB-ID 779519-1
    ISSN 1874-1754 ; 0167-5273
    ISSN (online) 1874-1754
    ISSN 0167-5273
    DOI 10.1016/j.ijcard.2018.05.049
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  3. Article ; Online: Comment on "Evaluating the cardiovascular safety of sclerostin inhibition using evidence from meta-analysis of clinical trials and human genetics".

    Hólm, Hilma / Sulem, Patrick / Tragante, Vinicius / Thorsteinsdottir, Unnur / Gudbjartsson, Daniel F / Stefansson, Kari

    Science translational medicine

    2021  Volume 13, Issue 622, Page(s) eabe8497

    Abstract: Genetic data do not provide evidence for SOST inhibition causing cardiovascular disease. ...

    Abstract Genetic data do not provide evidence for SOST inhibition causing cardiovascular disease.
    MeSH term(s) Adaptor Proteins, Signal Transducing/genetics ; Cardiovascular Diseases/genetics ; Human Genetics ; Humans
    Chemical Substances Adaptor Proteins, Signal Transducing
    Language English
    Publishing date 2021-12-01
    Publishing country United States
    Document type Journal Article ; Comment
    ZDB-ID 2518854-9
    ISSN 1946-6242 ; 1946-6234
    ISSN (online) 1946-6242
    ISSN 1946-6234
    DOI 10.1126/scitranslmed.abe8497
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  4. Article ; Online: Mendelian Randomization Study of ACLY and Cardiovascular Disease.

    Hólm, Hilma / Sulem, Patrick / Helgadóttir, Anna / Tragante, Vinicius / Þorleifsson, Guðmar / Guðbjartsson, Daníel / Stefánsson, Kári

    The New England journal of medicine

    2020  Volume 383, Issue 7, Page(s) e50

    MeSH term(s) Cardiovascular Diseases ; Genetic Predisposition to Disease ; Humans ; Mendelian Randomization Analysis
    Language English
    Publishing date 2020-08-06
    Publishing country United States
    Document type Letter ; Comment
    ZDB-ID 207154-x
    ISSN 1533-4406 ; 0028-4793
    ISSN (online) 1533-4406
    ISSN 0028-4793
    DOI 10.1056/NEJMc1908496
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  5. Article ; Online: Effect of tissue-grouped regulatory variants associated to type 2 diabetes in related secondary outcomes.

    Hemerich, Daiane / Smit, Roelof A J / Preuss, Michael / Stalbow, Lauren / van der Laan, Sander W / Asselbergs, Folkert W / van Setten, Jessica / Tragante, Vinicius

    Scientific reports

    2023  Volume 13, Issue 1, Page(s) 3579

    Abstract: Genome-wide association studies have identified over five hundred loci that contribute to variation in type 2 diabetes (T2D), an established risk factor for many diseases. However, the mechanisms and extent through which these loci contribute to ... ...

    Abstract Genome-wide association studies have identified over five hundred loci that contribute to variation in type 2 diabetes (T2D), an established risk factor for many diseases. However, the mechanisms and extent through which these loci contribute to subsequent outcomes remain elusive. We hypothesized that combinations of T2D-associated variants acting on tissue-specific regulatory elements might account for greater risk for tissue-specific outcomes, leading to diversity in T2D disease progression. We searched for T2D-associated variants acting on regulatory elements and expression quantitative trait loci (eQTLs) in nine tissues. We used T2D tissue-grouped variant sets as genetic instruments to conduct 2-Sample Mendelian Randomization (MR) in ten related outcomes whose risk is increased by T2D using the FinnGen cohort. We performed PheWAS analysis to investigate whether the T2D tissue-grouped variant sets had specific predicted disease signatures. We identified an average of 176 variants acting in nine tissues implicated in T2D, and an average of 30 variants acting on regulatory elements that are unique to the nine tissues of interest. In 2-Sample MR analyses, all subsets of regulatory variants acting in different tissues were associated with increased risk of the ten secondary outcomes studied on similar levels. No tissue-grouped variant set was associated with an outcome significantly more than other tissue-grouped variant sets. We did not identify different disease progression profiles based on tissue-specific regulatory and transcriptome information. Bigger sample sizes and other layers of regulatory information in critical tissues may help identify subsets of T2D variants that are implicated in certain secondary outcomes, uncovering system-specific disease progression.
    MeSH term(s) Humans ; Acceptance and Commitment Therapy ; Diabetes Mellitus, Type 2/genetics ; Disease Progression ; Genome-Wide Association Study ; Risk Factors ; Mendelian Randomization Analysis
    Language English
    Publishing date 2023-03-02
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2615211-3
    ISSN 2045-2322 ; 2045-2322
    ISSN (online) 2045-2322
    ISSN 2045-2322
    DOI 10.1038/s41598-023-30369-6
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  6. Article ; Online: Polygenic risk scores associate with blood pressure traits across the lifespan.

    Øvretveit, Karsten / Ingeström, Emma M L / Spitieris, Michail / Tragante, Vinicius / Wade, Kaitlin H / Thomas, Laurent F / Wolford, Brooke N / Wisløff, Ulrik / Gudbjartsson, Daniel F / Holm, Hilma / Stefansson, Kari / Brumpton, Ben M / Hveem, Kristian

    European journal of preventive cardiology

    2023  Volume 31, Issue 6, Page(s) 644–654

    Abstract: Aims: Hypertension is a major modifiable cause of morbidity and mortality that affects over 1 billion people worldwide. Blood pressure (BP) traits have a strong genetic component that can be quantified with polygenic risk scores (PRSs). To date, the ... ...

    Abstract Aims: Hypertension is a major modifiable cause of morbidity and mortality that affects over 1 billion people worldwide. Blood pressure (BP) traits have a strong genetic component that can be quantified with polygenic risk scores (PRSs). To date, the performance of BP PRSs has mainly been assessed in adults, and less is known about polygenic hypertension risk in childhood.
    Methods and results: Multiple PRSs for systolic BP (SBP), diastolic BP (DBP), and pulse pressure were developed using either genome-wide significant weights, pruning and thresholding, or Bayesian regression. Among 87 total PRSs, the top performer for each trait was applied in independent cohorts of children and adult to assess genotype-phenotype associations and disease risk across the lifespan. Differences between those with low (1st decile), average (2nd-9th decile), and high (10th decile) PRS emerge in the first years of life and are maintained throughout adulthood. These diverging BP trajectories also seem to affect cardiovascular and renal disease risk, with increased risk observed among those in the top decile and reduced risk among those in the bottom decile of the polygenic risk distribution compared with the rest of the population.
    Conclusion: Genetic risk factors are associated with BP traits across the lifespan, beginning in the first years of life. Given the importance of exposure time in disease pathogenesis and the early rise in BP levels among those genetically susceptible, PRSs may help identify high-risk individuals prior to hypertension onset, facilitate primordial prevention, and reduce the burden of this public health challenge.
    MeSH term(s) Adult ; Child ; Humans ; Blood Pressure ; Genetic Risk Score ; Longevity ; Bayes Theorem ; Hypertension/epidemiology ; Genetic Predisposition to Disease ; Risk Factors
    Language English
    Publishing date 2023-11-22
    Publishing country England
    Document type Journal Article
    ZDB-ID 2626011-6
    ISSN 2047-4881 ; 2047-4873
    ISSN (online) 2047-4881
    ISSN 2047-4873
    DOI 10.1093/eurjpc/zwad365
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  7. Article: Integrative Bioinformatics Approaches for Identification of Drug Targets in Hypertension.

    Hemerich, Daiane / van Setten, Jessica / Tragante, Vinicius / Asselbergs, Folkert W

    Frontiers in cardiovascular medicine

    2018  Volume 5, Page(s) 25

    Abstract: High blood pressure or hypertension is an established risk factor for a myriad of cardiovascular diseases. Genome-wide association studies have successfully found over nine hundred loci that contribute to blood pressure. However, the mechanisms through ... ...

    Abstract High blood pressure or hypertension is an established risk factor for a myriad of cardiovascular diseases. Genome-wide association studies have successfully found over nine hundred loci that contribute to blood pressure. However, the mechanisms through which these loci contribute to disease are still relatively undetermined as less than 10% of hypertension-associated variants are located in coding regions. Phenotypic cell-type specificity analyses and expression quantitative trait loci show predominant vascular and cardiac tissue involvement for blood pressure-associated variants. Maps of chromosomal conformation and expression quantitative trait loci (eQTL) in critical tissues identified 2,424 genes interacting with blood pressure-associated loci, of which 517 are druggable. Integrating genome, regulome and transcriptome information in relevant cell-types could help to functionally annotate blood pressure associated loci and identify drug targets.
    Language English
    Publishing date 2018-04-04
    Publishing country Switzerland
    Document type Journal Article
    ZDB-ID 2781496-8
    ISSN 2297-055X
    ISSN 2297-055X
    DOI 10.3389/fcvm.2018.00025
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  8. Article: Rare variant associations with birth weight identify genes involved in adipose tissue regulation, placental function and insulin-like growth factor signalling.

    Kentistou, Katherine A / Lim, Brandon E M / Kaisinger, Lena R / Steinthorsdottir, Valgerdur / Sharp, Luke N / Patel, Kashyap A / Tragante, Vinicius / Hawkes, Gareth / Gardner, Eugene J / Olafsdottir, Thorhildur / Wood, Andrew R / Zhao, Yajie / Thorleifsson, Gudmar / Day, Felix R / Ozanne, Susan E / Hattersley, Andrew T / O'Rahilly, Stephen / Stefansson, Kari / Ong, Ken K /
    Beaumont, Robin N / Perry, John R B / Freathy, Rachel M

    medRxiv : the preprint server for health sciences

    2024  

    Abstract: Investigating the genetic factors influencing human birth weight may lead to biological insights into fetal growth and long-term health. Genome-wide association studies of birth weight have highlighted associated variants in more than 200 regions of the ... ...

    Abstract Investigating the genetic factors influencing human birth weight may lead to biological insights into fetal growth and long-term health. Genome-wide association studies of birth weight have highlighted associated variants in more than 200 regions of the genome, but the causal genes are mostly unknown. Rare genetic variants with robust evidence of association are more likely to point to causal genes, but to date, only a few rare variants are known to influence birth weight. We aimed to identify genes that harbour rare variants that impact birth weight when carried by either the fetus or the mother, by analysing whole exome sequence data in UK Biobank participants. We annotated rare (minor allele frequency <0.1%) protein-truncating or high impact missense variants on whole exome sequence data in up to 234,675 participants with data on their own birth weight (fetal variants), and up to 181,883 mothers who reported the birth weight of their first child (maternal variants). Variants within each gene were collapsed to perform gene burden tests and for each associated gene, we compared the observed fetal and maternal effects. We identified 8 genes with evidence of rare fetal variant effects on birth weight, of which 2 also showed maternal effects. One additional gene showed evidence of maternal effects only. We observed 10/11 directionally concordant associations in an independent sample of up to 45,622 individuals (sign test
    Language English
    Publishing date 2024-04-03
    Publishing country United States
    Document type Preprint
    DOI 10.1101/2024.04.03.24305248
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  9. Article ; Online: The ENCODE project and perspectives on pathways.

    Tragante, Vinicius / Moore, Jason H / Asselbergs, Folkert W

    Genetic epidemiology

    2014  Volume 38, Issue 4, Page(s) 275–280

    Abstract: The recently completed ENCODE project is a new source of information on metabolic activity, unveiling knowledge about evolution and similarities among species, refuting the myth that most DNA is "junk" and has no actual function. With this expansive ... ...

    Abstract The recently completed ENCODE project is a new source of information on metabolic activity, unveiling knowledge about evolution and similarities among species, refuting the myth that most DNA is "junk" and has no actual function. With this expansive resource comes a challenge: integrating these new layers of information into our current knowledge of single-nucleotide polymorphisms and previously described metabolic pathways with the aim of discovering new genes and pathways related to human diseases and traits. Further, we must determine which computational methods will be most useful in this pursuit. In this paper, we speculate over the possible methods that will emerge in this new, challenging field.
    MeSH term(s) Animals ; Artificial Intelligence ; Genome, Human/genetics ; Genomics ; Humans ; Metabolic Networks and Pathways/genetics ; Phenotype ; Polymorphism, Single Nucleotide/genetics
    Language English
    Publishing date 2014-05
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 605785-8
    ISSN 1098-2272 ; 0741-0395
    ISSN (online) 1098-2272
    ISSN 0741-0395
    DOI 10.1002/gepi.21802
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  10. Article ; Online: Screening for Rare Coding Variants That Associate With the QTc Interval in Iceland.

    Sveinbjornsson, Gardar / Benediktsdottir, Bara D / Sigfusson, Gunnlaugur / Norland, Kristjan / Davidsson, Olafur B / Thorolfsdottir, Rosa B / Tragante, Vinicius / Arnadottir, Gudny A / Jensson, Brynjar O / Katrinardottir, Hildigunnur / Fridriksdottir, Run / Gudmundsdottir, Hallbera / Aegisdottir, Hildur M / Fridriksson, Brynjar / Thorgeirsson, Gudmundur / Magnusson, Vidar / Oddsson, Asmundur / Sulem, Patrick / Gudbjartsson, Daniel F /
    Holm, Hilma / Arnar, David O / Stefansson, Kari

    Journal of the American Heart Association

    2023  Volume 12, Issue 14, Page(s) e029845

    Abstract: Background Long-QT syndrome (LQTS) is a cardiac repolarization abnormality that can lead to sudden cardiac death. The most common causes are rare coding variants in the ... ...

    Abstract Background Long-QT syndrome (LQTS) is a cardiac repolarization abnormality that can lead to sudden cardiac death. The most common causes are rare coding variants in the genes
    MeSH term(s) Humans ; Iceland/epidemiology ; KCNQ1 Potassium Channel/genetics ; Long QT Syndrome/diagnosis ; Long QT Syndrome/epidemiology ; Long QT Syndrome/genetics ; Death, Sudden, Cardiac/epidemiology ; Death, Sudden, Cardiac/etiology ; Electrocardiography ; Mutation
    Chemical Substances KCNQ1 Potassium Channel
    Language English
    Publishing date 2023-07-14
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2653953-6
    ISSN 2047-9980 ; 2047-9980
    ISSN (online) 2047-9980
    ISSN 2047-9980
    DOI 10.1161/JAHA.123.029845
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