Journal article
Human Plasma Lipidome Is Pleiotropically Associated With Cardiovascular Risk Factors and Death
Claire Bellis, Hemant Kulkarni, Manju Mamtani, Jack W Kent, Gerard Wong, Jacquelyn M Weir, Christopher K Barlow, Vincent Diego, Marcio Almeida, Thomas D Dyer, Harald HH Goering, Laura Almasy, Michael C Mahaney, Anthony G Comuzzie, Sarah Williams-Blangero, Peter J Meikle, John Blangero, Joanne E Curran
CIRCULATION-CARDIOVASCULAR GENETICS | LIPPINCOTT WILLIAMS & WILKINS | Published : 2014
Abstract
BACKGROUND: Cardiovascular disease (CVD) is the most common cause of death in the United States and is associated with a high economic burden. Prevention of CVD focuses on controlling or improving the lipid profile of patients at risk. The human lipidome is made up of thousands of ubiquitous lipid species. By studying biologically simple canonical lipid species, we investigated whether the lipidome is genetically redundant and whether its genetic influences can provide clinically relevant clues of CVD risk. METHODS AND RESULTS: We performed a genetic study of the human lipidome in 1212 individuals from 42 extended Mexican American families. High-throughput mass spectrometry enabled rapid cap..
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Awarded by National Institutes of Health (NIH)
Awarded by National Health and Medical Research Council of Australia
Awarded by NIH
Awarded by National Center for Research Resources
Awarded by Research Facilities Improvement Program from the National Center for Research Resources of NIH
Awarded by NATIONAL CENTER FOR RESEARCH RESOURCES
Awarded by NATIONAL HEART, LUNG, AND BLOOD INSTITUTE
Awarded by NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES
Awarded by NATIONAL INSTITUTE OF MENTAL HEALTH
Funding Acknowledgements
This work was supported in part by National Institutes of Health (NIH) grants R01 HL113323, R01 DK079169, and R01 DK088972; by National Health and Medical Research Council of Australia Grants 1029754 and 1042095; and by the OIS Program of the Victorian Government, Australia. Data collection for the San Antonio Family Heart Study was supported by NIH grant R01 HL045522. The development of the analytical methods and software used in this study was supported by NIH grant R37 MH059490. The AT&T Genomics Computing Center supercomputing facilities used for this work were supported in part by a gift from the AT&T Foundation and with support from the National Center for Research Resources Grant Number S10 RR029392. This investigation was conducted in facilities constructed with support from Research Facilities Improvement Program grants C06 RR013556 and C06 RR017515 from the National Center for Research Resources of NIH.