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Wain, L.V.* ; Shrine, N.* ; Artigas, M.S.* ; Erzurumluoglu, A.M.* ; Noyvert, B.* ; Bossini-Castillo, L.* ; Obeidat, M.* ; Henry, A.P.* ; Portelli, M.A.* ; Hall, R.J.* ; Billington, C.K.* ; Rimington, T.L.* ; Fenech, A.G.* ; John, C.* ; Blake, T.* ; Jackson, V.E.* ; Allen, R.J.* ; Prins, B.P.* ; Campbell, A.* ; Porteous, D.J.* ; Jarvelin, M.R.* ; Wielscher, M.* ; James, A.L.* ; Hui, J.* ; Wareham, N.J.* ; Zhao, J.H.* ; Wilson, J.F.* ; Joshi, P.K.* ; Stubbe, B.* ; Rawal, R. ; Schulz, H. ; Imboden, M.* ; Probst-Hensch, N.M.* ; Karrasch, S. ; Gieger, C. ; Deary, I.J.* ; Harris, S.E.* ; Marten, J.* ; Rudan, I.* ; Enroth, S.* ; Gyllensten, U.* ; Kerr, S.M.* ; Polasek, O.* ; Kähönen, M.* ; Surakka, I.* ; Vitart, V.* ; Hayward, C.* ; Lehtimäki, T.* ; Raitakari, O.T.* ; Evans, D.M* ; Henderson, A.J.* ; Pennell, C.E.* ; Wang, C.A.* ; Sly, P.D.* ; Wan, E.S.* ; Busch, R.* ; Hobbs, B.D.* ; Litonjua, A.A.* ; Sparrow, D.W.* ; Gulsvik, A.* ; Bakke, P.S.* ; Crapo, J.D.* ; Beaty, T.H.* ; Hansel, N.N.* ; Mathias, R.A.* ; Ruczinski, I.* ; Barnes, K.C.* ; Bossé, Y.* ; Joubert, P.* ; van den Berge, M.* ; Brandsma, C.A.* ; Paré, P.D.* ; Sin, D.D.* ; Nickle, D.C.* ; Hao, K.* ; Gottesman, O.* ; Dewey, F.E.* ; Bruse, S.E.* ; Carey, D.J.* ; Kirchner, H.L.* ; Jonsson, S.* ; Thorleifsson, G.* ; Jonsdottir, I.* ; Gislason, T.* ; Stefansson, K.* ; Schurmann, C.* ; Nadkarni, G.* ; Bottinger, E.P.* ; Loos, R.J.* ; Walters, R.G.* ; Chen, Z.* ; Millwood, I.Y.* ; Vaucher, J.* ; Kurmi, O.P.* ; Li, L.* ; Hansell, A.L.* ; Brightling, C.* ; Zeggini, E.* ; Cho, M.H.* ; Silverman, E.K.* ; Sayers, I.* ; Trynka, G.* ; Morris, A.P.* ; Strachan, D.P.* ; Hall, I.P.* ; Tobin, M.D.*

Genome-wide association analyses for lung function and chronic obstructive pulmonary disease identify new loci and potential druggable targets.

Nat. Genet. 49, 416-425 (2017)
Postprint DOI PMC
Open Access Green
Chronic obstructive pulmonary disease (COPD) is characterized by reduced lung function and is the third leading cause of death globally. Through genome-wide association discovery in 48,943 individuals, selected from extremes of the lung function distribution in UK Biobank, and follow-up in 95,375 individuals, we increased the yield of independent signals for lung function from 54 to 97. A genetic risk score was associated with COPD susceptibility (odds ratio per 1 s.d. of the risk score (∼6 alleles) (95% confidence interval) = 1.24 (1.20-1.27), P = 5.05 × 10(-49)), and we observed a 3.7-fold difference in COPD risk between individuals in the highest and lowest genetic risk score deciles in UK Biobank. The 97 signals show enrichment in genes for development, elastic fibers and epigenetic regulation pathways. We highlight targets for drugs and compounds in development for COPD and asthma (genes in the inositol phosphate metabolism pathway and CHRM3) and describe targets for potential drug repositioning from other clinical indications.
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Publikationstyp Artikel: Journalartikel
Dokumenttyp Wissenschaftlicher Artikel
Schlagwörter Air-flow Obstruction; Copd; Variants; Genetics; Susceptibility; Epidemiology; Population; History; Health; Fam13a
Sprache englisch
Veröffentlichungsjahr 2017
HGF-Berichtsjahr 2017
ISSN (print) / ISBN 1061-4036
e-ISSN 1546-1718
Zeitschrift Nature Genetics
Quellenangaben Band: 49, Heft: 3, Seiten: 416-425 Artikelnummer: , Supplement: ,
Verlag Nature Publishing Group
Verlagsort New York, NY
Begutachtungsstatus Peer reviewed
Institut(e) Institute of Genetic Epidemiology (IGE)
Institute of Epidemiology (EPI)
POF Topic(s) 30501 - Systemic Analysis of Genetic and Environmental Factors that Impact Health
30202 - Environmental Health
80000 - German Center for Lung Research
30503 - Chronic Diseases of the Lung and Allergies
Forschungsfeld(er) Genetics and Epidemiology
PSP-Element(e) G-504100-001
G-504000-009
G-504091-004
G-501800-391
G-503900-003
DOI 10.1038/ng.3787
WOS ID WOS:000394917800015
Scopus ID 85011684926
PubMed ID 28166213
Erfassungsdatum 2017-03-09
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