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E. and Oldehinkel, Albertine J. and Pereira, Alexandre C. and Perls, Thomas and Rauramaa, Rainer and Redline, Susan and Rettig, Rainer and Samani, Nilesh J. and Scott, James and Shu, Xiao-Ou and van Der Harst, Pim and Wagenknecht, Lynne E. and Wareham, Nicholas J. and Watkins, Hugh and Wickremasinghe, Ananda R. and Wu, Tangchun and Kamatani, Yoichiro and Laurie, Cathy C. and Bouchard, Claude and Cooper, Richard S. and Evans, Michele K. and Gudnason, Vilmundur and Hixson, James and Kardia, Sharon L. R. and Kritchevsky, Stephen B. and Psaty, Bruce M. and van Dam, Rob M. and Arnett, Donna K. and Mook-Kanamori, Dennis O. and Fornage, Myriam and Fox, Ervin R. and Hayward, Caroline and van Duijn, Cornelia M. and Tai, E. Shyong and Wong, Tien Yin and Loos, Ruth J. F. and Reiner, Alex P. and Rotimi, Charles N. and Bierut, Laura J. and Zhu, Xiaofeng and Cupples, L. Adrienne and Province, Michael A. and Rotter, Jerome and Franks, Paul W. and Rice, Kenneth and Elliott, Paul and Caulfield, Mark J. and Gauderman, W. James and Munroe, Patricia B. and Rao, Dabeeru C. and Morrison, Alanna C. (2019) A multi-ancestry genome-wide study incorporating gene-smoking interactions identifies multiple new loci for pulse pressure and mean arterial pressure. HUMAN MOLECULAR GENETICS, 28 (15). pp. 2615-2633. ISSN 0964-6906, 1460-2083
Full text not available from this repository. (Request a copy)Abstract
Elevated blood pressure (BP), a leading cause of global morbidity and mortality, is influenced by both genetic and lifestyle factors. Cigarette smoking is one such lifestyle factor. Across five ancestries, we performed a genome-wide gene-smoking interaction study of mean arterial pressure (MAP) and pulse pressure (PP) in 129 913 individuals in stage 1 and follow-up analysis in 480 178 additional individuals in stage 2. We report here 136 loci significantly associated with MAP and/or PP. Of these, 61 were previously published through main-effect analysis of BP traits, 37 were recently reported by us for systolic BP and/or diastolic BP through gene-smoking interaction analysis and 38 were newly identified (P < 5 x 10(-8), false discovery rate < 0.05). We also identified nine new signals near known loci. Of the 136 loci, 8 showed significant interaction with smoking status. They include CSMD1 previously reported for insulin resistance and BP in the spontaneously hypertensive rats. Many of the 38 new loci show biologic plausibility for a role in BP regulation. SLC26A7 encodes a chloride/bicarbonate exchanger expressed in the renal outer medullary collecting duct. AVPR1A is widely expressed, including in vascular smooth muscle cells, kidney, myocardium and brain. FHAD1 is a long non-coding RNA overexpressed in heart failure. TMEM51 was associated with contractile function in cardiomyocytes. CASP9 plays a central role in cardiomyocyte apoptosis. Identified only in African ancestry were 30 novel loci. Our findings highlight the value of multi-ancestry investigations, particularly in studies of interaction with lifestyle factors, where genomic and lifestyle differences may contribute to novel findings.
| Item Type: | Article |
|---|---|
| Uncontrolled Keywords: | HYDROCARBON RECEPTOR AHR; SYSTOLIC BLOOD-PRESSURE; BODY-MASS INDEX; ENVIRONMENT INTERACTION; DEPENDENT HYPERTENSION; CARDIOVASCULAR RISK; OXIDATIVE STRESS; T-CADHERIN; ASSOCIATION; METAANALYSIS; |
| Subjects: | 600 Technology > 610 Medical sciences Medicine |
| Divisions: | Medicine > Institut für Epidemiologie und Präventivmedizin Medicine > Institut für Epidemiologie und Präventivmedizin > Lehrstuhl für Genetische Epidemiologie |
| Depositing User: | Dr. Gernot Deinzer |
| Date Deposited: | 01 Apr 2020 07:42 |
| Last Modified: | 01 Apr 2020 07:42 |
| URI: | https://pred.uni-regensburg.de/id/eprint/26471 |
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