期刊
AMERICAN JOURNAL OF HUMAN GENETICS
卷 104, 期 1, 页码 157-163出版社
CELL PRESS
DOI: 10.1016/j.ajhg.2018.11.004
关键词
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资金
- UK Biobank [11867]
- European Commission Horizon 2020 research and innovation programme [692065]
- Novo Nordisk
- UK Medical Research Council
- British Heart Foundation Intermediate Clinical Research Fellowship [FS/18/23/33512]
- Li Ka Shing Foundation
- WT-SSI/John Fell funds, Oxford
- NIH [5P50HD028138-27]
- National Institute for Health Research Oxford Biomedical Research Centre
- Widenlife
- MRC [1946461] Funding Source: UKRI
Erectile dysfunction (ED) is a common condition affecting more than 20% of men over 60 years, yet little is known about its genetic architecture. We performed a genome-wide association study of ED in 6,175 case subjects among 223,805 European men and identified one locus at 6q16.3 (lead variant rs57989773, OR 1.20 per C-allele; p = 5.71 x 10(-14)), located between MCHR2 and SIM1. In silico analysis suggests SIM1 to confer ED risk through hypothalamic dysregulation. Mendelian randomization provides evidence that genetic risk of type 2 diabetes mellitus is a cause of ED (OR 1.11 per 1-log unit higher risk of type 2 diabetes). These findings provide insights into the biological underpinnings and the causes of ED and may help prioritize the development of future therapies for this common disorder.
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