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Cited by 625

The DOI matches its Crossref record; 22 of the 22 references it cites were found in a registry or an index.

Genetics of blood lipids among ∼300,000 multi-ethnic participants of the Million Veteran Program

Global Lipids Genetics Consortium, Klarin, Derek, Myocardial Infarction Genetics (MIGen) Consortium, The Geisinger-Regeneron DiscovEHR Collaboration, The VA Million Veteran Program, Damrauer, Scott M., Cho, Kelly, Sun, Yan V., Teslovich, Tanya M., Honerlaw, Jacqueline, Gagnon, David R., DuVall, Scott L., Li, Jin, Peloso, Gina M., Chaffin, Mark, Small, Aeron M., Huang, Jie, Tang, Hua, Lynch, Julie A., Ho, Yuk-Lam, Liu, Dajiang J., Emdin, Connor A., Li, Alexander H., Huffman, Jennifer E., Lee, Jennifer S., Natarajan, Pradeep, Chowdhury, Rajiv, Saleheen, Danish, Vujkovic, Marijana, Baras, Aris, Pyarajan, Saiju, Di Angelantonio, Emanuele, Neale, Benjamin M., Naheed, Aliya, Khera, Amit V., Danesh, John, Chang, Kyong-Mi, Abecasis, Gonçalo, Willer, Cristen, Dewey, Frederick E., Carey, David J., Concato, John, Gaziano, J. Michael, O’Donnell, Christopher J., Tsao, Philip S., Kathiresan, Sekar, Rader, Daniel J., Wilson, Peter W. F., Assimes, Themistocles L.·2018·Nature Genetics
DOI 10.1038/s41588-018-0222-9PMC PMC6521726
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Registry

Crossref · 10.1038/s41588-018-0222-9

Cites

22 of 22 references verified0 citation errors · 0 not checkable

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  • There are over 300 loci uncovered to be associated with plasma lipid levels in humans.

    “There are over 300 loci uncovered to be associated with plasma lipid levels in humans (Klarin et al., 2018; Liu et al., 2017; Teslovich et al., 2010; Willer et al., 2013).”

    From GPR146 Deficiency Protects against Hypercholesterolemia and Atherosclerosis (2019) · cites this paper as Klarin et al., 2018

  • Human genetic studies have unequivocally established GPR146 as a susceptible gene regulating plasma cholesterol levels.

    “Human genetic studies have unequivocally established GPR146 as a susceptible gene regulating plasma cholesterol levels.”

    From GPR146 Deficiency Protects against Hypercholesterolemia and Atherosclerosis (2019) · cites this paper as Klarin et al., 2018

    The Discussion describes genetic loci associated with blood lipids, but the passages do not identify GPR146 as one of them or establish that it regulates plasma cholesterol. Searches for “GPR146” and “G protein-coupled receptor 146” found no passage addressing that gene. (LLM, conf=0.72)

    Experimental — accuracy not yet measured

  • GPR146 is a susceptible gene associated with plasma total cholesterol (TC), LDL-C and HDL-C levels.

    “GPR146, a susceptible gene associated with plasma total cholesterol (TC), LDL-C and high density lipoprotein cholesterol (HDL-C) levels”

    From GPR146 Deficiency Protects against Hypercholesterolemia and Atherosclerosis (2019) · cites this paper as Klarin et al., 2018

    The Results passages on lipid associations discuss other genes, including PDE3B, but do not identify GPR146 as associated with total cholesterol, LDL-C, or HDL-C. Searches for “GPR146” and “GPR146 total cholesterol LDL-C HDL-C” found no passage addressing that gene; page numbers were not available in our copy. (LLM, conf=0.72)

    Experimental — accuracy not yet measured

  • The alternative allele of rs1997243-G, located 11-kb upstream of GPR146, is associated with increased plasma TC, HDL-C and LDL-C levels in humans.

    “The alternative allele of a common variant (rs1997243-G), located 11-kb upstream of GPR146, has been shown to be associated with increased plasma TC, HDL-C and LDL-C levels in humans (Klarin et al., 2018; Liu et al., 2017; Willer et al., 2013)”

    From GPR146 Deficiency Protects against Hypercholesterolemia and Atherosclerosis (2019) · cites this paper as Klarin et al., 2018

    The Results section on lipid genetic associations discusses other variants, but the passages from our copy do not identify rs1997243-G or GPR146. Searches for both terms and for the claimed upstream location and lipid associations found no passage establishing this specific claim; the other papers cited in the sentence were not assessed. (LLM, conf=0.73)

    Experimental — accuracy not yet measured

  • Loss of function PCSK9 is associated with reduced CVD due to LDLR stabilization.

    “Loss of function PCSK9 is associated with reduced CVD due to LDLR stabilization130,131.”

    From Pathways and Molecular Mechanisms Governing LDL Receptor Regulation (2025) · cites this paper as [131]

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Citations

Cites

Flagged first, then by citations

Research works printed but not linked: 37

  1. Collins, R. What makes UK Biobank special? Lancet 379, 1173–1174 (2012). · DOI · Paper page
  2. Gaziano, J. M. et al. Million Veteran Program: a mega-biobank to study genetic influences on health and disease. J. Clin. Epidemiol. 70, 214–223 (2016). · DOI · Paper page
  3. The Emerging Risk Factors Collaboration. Major lipids, apolipoproteins, and risk of vascular disease. J. Am. Med. Assoc. 302, 1993–2000 (2009). · DOI · Paper page
  4. Global Lipids Genetics Consortium.. Discovery and refinement of loci associated with lipid levels. Nat. Genet. 45, 1274–1283 (2013). · DOI
  5. Albrechtsen, A. et al. Exome sequencing-driven discovery of coding polymorphisms associated with common metabolic phenotypes. Diabetologia 56, 298–310 (2013). · DOI
  6. Peloso, G. M. et al. Association of low-frequency and rare coding-sequence variants with blood lipids and coronary heart disease in 56,000 whites and blacks. Am. J. Hum. Genet. 94, 223–232 (2014). · DOI
  7. Asselbergs, F. W. et al. Large-scale gene-centric meta-analysis across 32 studies identifies multiple lipid loci. Am. J. Hum. Genet. 91, 823–838 (2012). · DOI
  8. Below, J. E. et al. Meta-analysis of lipid-traits in Hispanics identifies novel loci, population-specific effects, and tissue-specific enrichment of eQTLs. Sci. Rep. 6, 19429 (2016). · DOI
  9. Liu, D. J. et al. Exome-wide association study of plasma lipids in >300,000 individuals. Nat. Genet. 49, 1758–1766 (2017). · DOI · Paper page
  10. Lu, X. et al. Exome chip meta-analysis identifies novel loci and East Asian-specific coding variants that contribute to lipid levels and coronary artery disease. Nat. Genet. 49, 1722–1730 (2017). · DOI
  11. Denny, J. C. et al. Systematic comparison of phenome-wide association study of electronic medical record data and genome-wide association study data. Nat. Biotechnol. 31, 1102–1111 (2013). · DOI
  12. Gusev, A. et al. Integrative approaches for large-scale transcriptome-wide association studies. Nat. Genet. 48, 245–252 (2016). · DOI · Paper page
  13. Mancuso, N. et al. Integrating gene expression with summary association statistics to identify genes associated with 30 complex traits. Am. J. Hum. Genet. 100, 473–487 (2017). · DOI
  14. McLaren, W. et al. Deriving the consequences of genomic variants with the Ensembl API and SNP Effect Predictor. Bioinformatics 26, 2069–2070 (2010). · DOI
  15. Dewey, F. E. et al. Distribution and clinical impact of functional variants in 50,726 whole-exome sequences from the DiscovEHR study. Science 354, aaf6814 (2016). · DOI
  16. Sidore, C. et al. Genome sequencing elucidates Sardinian genetic architecture and augments association analyses for lipid and blood inflammatory markers. Nat. Genet. 47, 1272–1281 (2015). · DOI
  17. Diogo, D. et al. Phenome-wide association studies (PheWAS) across large “real-world data” population cohorts support drug target validation. Preprint at https://www.biorxiv.org/content/early/2017/11/13/218875 (2017). · DOI
  18. Mahajan, A. et al. Refining the accuracy of validated target identification through coding variant fine-mapping in type 2 diabetes. Nat. Genet. 50, 559–571 (2018). · DOI · Paper page
  19. Nelson, C. P. et al. Association analyses based on false discovery rate implicate new loci for coronary artery disease. Nat. Genet. 49, 1385–1391 (2017). · DOI
  20. Gandotra, S. et al. Perilipin deficiency and autosomal dominant partial lipodystrophy. N. Engl. J. Med. 364, 740–748 (2011). · DOI
  21. Rani, J. et al. T2DiACoD: a gene atlas of type 2 diabetes mellitus associated complex disorders. Sci. Rep. 7, 6892 (2017). · DOI
  22. Musunuru, K. et al. Exome sequencing, ANGPTL3 mutations, and familial combined hypolipidemia. N. Engl. J. Med. 363, 2220–2227 (2010). · DOI · Paper page
  23. Zhang, W. & Colman, R. W. Thrombin regulates intracellular cyclic AMP concentration in human platelets through phosphorylation/activation of phosphodiesterase 3A. Blood 110, 1475–1482 (2007). · DOI
  24. Maass, P. G. et al. PDE3A mutations cause autosomal dominant hypertension with brachydactyly. Nat. Genet. 47, 647–653 (2015). · DOI · Paper page
  25. Vandeput, F. et al. Selective regulation of cyclic nucleotide phosphodiesterase PDE3A isoforms. Proc. Natl Acad. Sci. USA 110, 19778–19783 (2013). · DOI
  26. Bedenis, R. et al. Cilostazol for intermittent claudication. Cochrane Database Syst. Rev. 10, CD003748 (2014).
  27. Tsuchikane, E. et al. Impact of cilostazol on restenosis after percutaneous coronary balloon angioplasty. Circulation 100, 21–26 (1999). · DOI
  28. Shinohara, Y. et al. Cilostazol for prevention of secondary stroke (CSPS 2): an aspirin-controlled, double-blind, randomised non-inferiority trial. Lancet Neurol. 9, 959–968 (2010). · DOI
  29. Ahmad, F. et al. Phosphodiesterase 3B (PDE3B) regulates NLRP3 inflammasome in adipose tissue. Sci. Rep. 6, 28056 (2016). · DOI
  30. Chung, Y. W. et al. Targeted disruption of PDE3B, but not PDE3A, protects murine heart from ischemia/reperfusion injury. Proc. Natl Acad. Sci. USA 112, E2253–E2262 (2015). · DOI
  31. Harrison, S. C. et al. Genetic association of lipids and lipid drug targets with abdominal aortic aneurysm: a meta-analysis. JAMA Cardiol. 3, 26–33 (2018). · DOI
  32. Lu, H. et al. Hypercholesterolemia induced by a PCSK9 gain-of-function mutation augments angiotensin II-induced abdominal aortic aneurysms in C57BL/6 mice—brief report. Arterioscler. Thromb. Vasc. Biol. 36, 1753–1757 (2016). · DOI
  33. Voight, B. F. et al. Plasma HDL cholesterol and risk of myocardial infarction: a mendelian randomisation study. Lancet 380, 572–580 (2012). · DOI · Paper page
  34. Do, R. et al. Common variants associated with plasma triglycerides and risk for coronary artery disease. Nat. Genet. 45, 1345–1352 (2013). · DOI · Paper page
  35. Loh, P. R., Palamara, P. F. & Price, A. L. Fast and accurate long-range phasing in a UK Biobank cohort. Nat. Genet. 48, 811–816 (2016). · DOI · Paper page
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Metadata

Authors
Global Lipids Genetics Consortium, Klarin, D., Myocardial Infarction Genetics (MIGen) Consortium, The Geisinger-Regeneron DiscovEHR Collaboration, Program, T. V. M. V., Damrauer, S. M., Cho, K., Sun, Y. V., Teslovich, T. M., Honerlaw, J., Gagnon, D. R., DuVall, S. L., Li, J., Peloso, G. M., Chaffin, M., Small, A. M., Huang, J., Tang, H., Lynch, J. A., Ho, Y.-L., Liu, D. J., Emdin, C. A., Li, A. H., Huffman, J. E., Lee, J. S., Natarajan, P., Chowdhury, R., Saleheen, D., Vujkovic, M., Baras, A., Pyarajan, S., Di Angelantonio, E., Neale, B. M., Naheed, A., Khera, A. V., Danesh, J., Chang, K.-M., Abecasis, G., Willer, C., Dewey, F. E., Carey, D. J., Concato, J., Gaziano, J. M., O’Donnell, C. J., Tsao, P. S., Kathiresan, S., Rader, D. J., Wilson, P. W. F., & Assimes, T. L.
ORCID
Venue
Nature Genetics
Publisher
Springer Science and Business Media LLC
Published
2018-10-01
Volume
50
Issue
11
Pages
1514-1523
ISSN
  • 1061-4036
  • 1546-1718
DOI
10.1038/s41588-018-0222-9
PMC
PMC6521726
Cited by
625
References
22
Language
en
Licence
www.springer.com/tdm (tdm)

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