Jonathan C. Cohen, PhD Journal of Clinical Lipidology

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Emerging LDL therapies: Using human genetics to discover new therapeutic targets for plasma lipids Jonathan C. Cohen, PhD Journal of Clinical Lipidology Volume 7, Issue 3, Pages S1-S5 (May 2013) DOI: 10.1016/j.jacl.2013.03.005 Copyright © 2013 National Lipid Association Terms and Conditions

Figure 1 Schematic of the relationship between allele frequency and effect size. APOB, gene for apolipoprotein B; APOE, gene for apolipoprotein E; LDL-C, low-density lipoprotein cholesterol; LDLR, gene for low-density lipoprotein receptor; PCSK9, gene for proprotein convertase subtilisin/kexin type 9; SORT1, gene for sortilin 1. Journal of Clinical Lipidology 2013 7, S1-S5DOI: (10.1016/j.jacl.2013.03.005) Copyright © 2013 National Lipid Association Terms and Conditions

Figure 2 Hazard ratios of myocardial infarction in prospective studies (n = 25,000) per standard deviation increase in lipid level. Plasma denotes predicted hazard ratios for the change in plasma levels of each lipoprotein that would be caused by the SNPs.17 HDL, high-density lipoprotein; LDL, low-density lipoprotein; SNPs, single nucleotide polymorphisms. Journal of Clinical Lipidology 2013 7, S1-S5DOI: (10.1016/j.jacl.2013.03.005) Copyright © 2013 National Lipid Association Terms and Conditions

Figure 3 Reduction in coronary heart disease associated with LDL-C lowering according to gene variants or statin use.1,22 APOB, gene for apolipoprotein B; CHD, coronary heart disease; LDL-C, low-density lipoprotein cholestrol; LDLR, gene for low-density lipoprotein receptor; PCSK9, gene for proprotein convertase subtilisin/kexin type 9; SORT1, gene for sortilin 1. Journal of Clinical Lipidology 2013 7, S1-S5DOI: (10.1016/j.jacl.2013.03.005) Copyright © 2013 National Lipid Association Terms and Conditions