Plasma lipids — such as cholesterol and triglycerides, and plasma lipoproteins such as low-density lipoprotein (LDL) and high-density lipoprotein (HDL) — are among the most important risk factors for cardiovascular disease.
Progress in understanding the genes determining plasma lipoprotein levels has rapidly accelerated owing to high-throughput automated DNA sequencing and genome-wide association analysis.
Phenomic analysis (or deep phenotyping) allows lipoprotein phenotype data to be analysed as part of a continuum that includes biochemical and molecular data.
Genetic determinants of plasma lipoprotein levels seem to conform to a mosaic model, involving contributions from multiple DNA sequence variants, both rare and common, with a range of effect sizes.
Many of the same genes in which rare mutations cause extreme and uncommon syndromes or diseases of lipoprotein metabolism also contain common variants with more subtle effects on plasma lipoprotein levels in the normal range.
In addition to increasing our understanding of plasma lipoprotein metabolism, the identification by genetics of new pathways and targets is likely to inform new drug design and could eventually lead to evidence-based changes in practice.
Susceptibility to the growing global public health problem of cardiovascular disease is associated with levels of plasma lipids and lipoproteins. Several experimental strategies have helped us to clarify the genetic architecture of these complex traits, including classical studies of monogenic dyslipidaemias, resequencing, phenomic analysis and, more recently, genome-wide association studies and analysis of metabolic networks. The genetic basis of plasma lipoprotein levels can now be modelled as a mosaic of contributions from multiple DNA sequence variants, both rare and common, with varying effect sizes. In addition to filling gaps in our understanding of plasma lipoprotein metabolism, the recent genetic advances will improve our ability to classify, diagnose and treat dyslipidaemias.
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Breslow, J. L. Genetics of lipoprotein abnormalities associated with coronary artery disease susceptibility. Annu. Rev. Genet. 34, 233–254 (2000).
Lusis, A. J. Genetic factors affecting blood lipoproteins: the candidate gene approach. J. Lipid Res. 29, 397–429 (1988).
Cohen, J. C. et al. Multiple rare alleles contribute to low plasma levels of HDL cholesterol. Science 305, 869–872 (2004). An early demonstration of how resequencing individuals at the extremes of the distribution of lipoprotein levels can uncover genetic determinants.
Brown, M. S. & Goldstein, J. L. A receptor-mediated pathway for cholesterol homeostasis. Science 232, 34–47 (1986).
Incardona, J. P. & Roelink, H. The role of cholesterol in Shh signaling and teratogen-induced holoprosencephaly. Cell. Mol. Life Sci. 57, 1709–1719 (2000).
Repa, J. J. & Mangelsdorf, D. J. The role of orphan nuclear receptors in the regulation of cholesterol homeostasis. Annu. Rev. Cell Dev. Biol. 16, 459–481 (2000).
Lusis, A. J. Atherosclerosis. Nature 407, 233–241 (2000).
Rader, D. J. & Daugherty, A. Translating molecular discoveries into new therapies for atherosclerosis. Nature 451, 904–913 (2008).
Grundy, S. M. Promise of low-density lipoprotein-lowering therapy for primary and secondary prevention. Circulation 117, 569–573; discussion 573 (2008).
Lewis, G. F. & Rader, D. J. New insights into the regulation of HDL metabolism and reverse cholesterol transport. Circ. Res. 96, 1221–1232 (2005).
Stamler, J. et al. Relationship of baseline serum cholesterol levels in 3 large cohorts of younger men to long-term coronary, cardiovascular, and all-cause mortality and to longevity. JAMA 284, 311–318 (2000).
Genest, J. J. Jr et al. Familial lipoprotein disorders in patients with premature coronary artery disease. Circulation 85, 2025–2033 (1992).
Sniderman, A. D. Applying apoB to the diagnosis and therapy of the atherogenic dyslipoproteinemias: a clinical diagnostic algorithm. Curr. Opin. Lipidol. 15, 433–438 (2004).
Barter, P. J. & Rye, K. A. The rationale for using apoA-I as a clinical marker of cardiovascular risk. J. Intern. Med. 259, 447–454 (2006).
McQueen, M. J. et al. Lipids, lipoproteins, and apolipoproteins as risk markers of myocardial infarction in 52 countries (the INTERHEART study): a case–control study. Lancet 372, 224–233 (2008).
van der Steeg, W. A. et al. Role of the apolipoprotein B–apolipoprotein A-I ratio in cardiovascular risk assessment: a case–control analysis in EPIC-Norfolk. Ann. Intern. Med. 146, 640–648 (2007).
Nordestgaard, B. G., Benn, M., Schnohr, P. & Tybjaerg-Hansen, A. Nonfasting triglycerides and risk of myocardial infarction, ischemic heart disease, and death in men and women. JAMA 298, 299–308 (2007).
Bansal, S. et al. Fasting compared with nonfasting triglycerides and risk of cardiovascular events in women. JAMA 298, 309–316 (2007).
Austin, M. A. et al. Cardiovascular disease mortality in familial forms of hypertriglyceridemia: a 20-year prospective study. Circulation 101, 2777–2782 (2000).
Kathiresan, S. et al. Six new loci associated with blood low-density lipoprotein cholesterol, high-density lipoprotein cholesterol or triglycerides in humans. Nature Genet. 40, 189–197 (2008).
Kooner, J. S. et al. Genome-wide scan identifies variation in MLXIPL associated with plasma triglycerides. Nature Genet. 40, 149–151 (2008).
Sandhu, M. S. et al. LDL-cholesterol concentrations: a genome-wide association study. Lancet 371, 483–491 (2008).
Wallace, C. et al. Genome-wide association study identifies genes for biomarkers of cardiovascular disease: serum urate and dyslipidemia. Am. J. Hum. Genet. 82, 139–149 (2008).
Willer, C. J. et al. Newly identified loci that influence lipid concentrations and risk of coronary artery disease. Nature Genet. 40, 161–169 (2008).
Aulchenko, Y. S. et al. Genome-wide association study in 16 European population cohorts: major loci influencing lipid levels and coronary heart disease risk. Nature Genet. 41, 47–55 (2009).
Kathiresan, S. et al. Common DNA sequence variants at thirty genetic loci contribute to polygenic dyslipidemia. Nature Genet. 41, 56–65 (2009).
Sabatti, C. et al. Genomewide association analysis of metabolic traits in a birth cohort from a founder population. Nature Genet. 41, 35–46 (2009). References 20–27 are GWA studies that identify new loci for plasma lipoproteins.
Hegele, R. A., Brunt, J. H. & Connelly, P. W. Multiple genetic determinants of variation of plasma lipoproteins in Alberta Hutterites. Arterioscler. Thromb. Vasc. Biol. 15, 861–871 (1995).
Pajukanta, P. et al. Familial combined hyperlipidemia is associated with upstream transcription factor 1 (USF1). Nature Genet. 36, 371–376 (2004).
Lee, J. C. et al. WW-domain-containing oxidoreductase is associated with low plasma HDL-C levels. Am. J. Hum. Genet. 83, 180–192 (2008).
Saxena, R. et al. Genome-wide association analysis identifies loci for type 2 diabetes and triglyceride levels. Science 316, 1331–1336 (2007).
Bennet, A. M. et al. Association of apolipoprotein E genotypes with lipid levels and coronary risk. JAMA 298, 1300–1311 (2007).
Thompson, A. et al. Association of cholesteryl ester transfer protein genotypes with CETP mass and activity, lipid levels, and coronary risk. JAMA 299, 2777–2788 (2008).
Shoulders, C. C., Jones, E. L. & Naoumova, R. P. Genetics of familial combined hyperlipidemia and risk of coronary heart disease. Hum. Mol. Genet. 13, R149–R160 (2004).
Pollex, R. L. & Hegele, R. A. Genetic determinants of plasma lipoproteins. Nature Clin. Pract. Cardiovasc. Med. 4, 600–609 (2007).
Rader, D. J., Cohen, J. & Hobbs, H. H. Monogenic hypercholesterolemia: new insights in pathogenesis and treatment. J. Clin. Invest. 111, 1795–1803 (2003).
Tarugi, P. et al. Molecular diagnosis of hypobetalipoproteinemia: an ENID review. Atherosclerosis 195, e19–e27 (2007).
Brooks-Wilson, A. et al. Mutations in ABC1 in Tangier disease and familial high-density lipoprotein deficiency. Nature Genet. 22, 336–345 (1999).
Assmann, G., von Eckardstein, A. & Funke, H. High density lipoproteins, reverse transport of cholesterol, and coronary artery disease. Insights from mutations. Circulation 87, III28–III34 (1993).
Hovingh, G. K. et al. Inherited disorders of HDL metabolism and atherosclerosis. Curr. Opin. Lipidol. 16, 139–145 (2005).
Fojo, S. S. & Brewer, H. B. Hypertriglyceridaemia due to genetic defects in lipoprotein lipase and apolipoprotein C-II. J. Intern. Med. 231, 669–677 (1992).
Peterfy, M. et al. Mutations in LMF1 cause combined lipase deficiency and severe hypertriglyceridemia. Nature Genet. 39, 1483–1487 (2007).
Young, S. G. et al. GPIHBP1: an endothelial cell molecule important for the lipolytic processing of chylomicrons. Curr. Opin. Lipidol. 18, 389–396 (2007).
Talmud, P. J. Rare APOA5 mutations — clinical consequences, metabolic and functional effects: an ENID review. Atherosclerosis 194, 287–292 (2007).
Stroes, E. S. et al. Intramuscular administration of AAV1-lipoprotein lipase S447X lowers triglycerides in lipoprotein lipase-deficient patients. Arterioscler. Thromb. Vasc. Biol. 28, 2303–2304 (2008).
Whitfield, A. J., Barrett, P. H., van Bockxmeer, F. M. & Burnett, J. R. Lipid disorders and mutations in the APOB gene. Clin. Chem. 50, 1725–1732 (2004).
Jones, B. et al. Mutations in a Sar1 GTPase of COPII vesicles are associated with lipid absorption disorders. Nature Genet. 34, 29–31 (2003).
Ahituv, N. et al. Medical sequencing at the extremes of human body mass. Am. J. Hum. Genet. 80, 779–791 (2007).
Kryukov, G. V., Pennacchio, L. A. & Sunyaev, S. R. Most rare missense alleles are deleterious in humans: implications for complex disease and association studies. Am. J. Hum. Genet. 80, 727–739 (2007).
Cohen, J. et al. Low LDL cholesterol in individuals of African descent resulting from frequent nonsense mutations in PCSK9. Nature Genet. 37, 161–165 (2005).
Cohen, J. C. et al. Multiple rare variants in NPC1L1 associated with reduced sterol absorption and plasma low-density lipoprotein levels. Proc. Natl Acad. Sci. USA 103, 1810–1815 (2006).
Fahmi, S., Yang, C., Esmail, S., Hobbs, H. H. & Cohen, J. C. Functional characterization of genetic variants in NPC1L1 supports the sequencing extremes strategy to identify complex trait genes. Hum. Mol. Genet. 17, 2101–7 (2008).
Wang, J. et al. Resequencing genomic DNA of patients with severe hypertriglyceridemia (MIM 144650). Arterioscler. Thromb. Vasc. Biol. 27, 2450–2455 (2007).
deLemos, A. S., Wolfe, M. L., Long, C. J., Sivapackianathan, R. & Rader, D. J. Identification of genetic variants in endothelial lipase in persons with elevated high-density lipoprotein cholesterol. Circulation 106, 1321–1326 (2002).
Yoshida, K., Shimizugawa, T., Ono, M. & Furukawa, H. Angiopoietin-like protein 4 is a potent hyperlipidemia-inducing factor in mice and inhibitor of lipoprotein lipase. J. Lipid Res. 43, 1770–1772 (2002).
Romeo, S. et al. Population-based resequencing of ANGPTL4 uncovers variations that reduce triglycerides and increase HDL. Nature Genet. 39, 513–516 (2007).
Frazer, K. A. et al. A second generation human haplotype map of over 3.1 million SNPs. Nature 449, 851–861 (2007).
Kathiresan, S. et al. A genome-wide association study for blood lipid phenotypes in the Framingham Heart Study. BMC Med. Genet. 8 (Suppl. 1), S17 (2007).
Hunter, D. J., Altshuler, D. & Rader, D. J. From Darwin's finches to canaries in the coal mine — mining the genome for new biology. N. Engl. J. Med. 358, 2760–2763 (2008).
Kathiresan, S., Musunuru, K. & Orho-Melander, M. Defining the spectrum of alleles that contribute to blood lipid concentrations in humans. Curr. Opin. Lipidol. 19, 122–127 (2008).
Krauss, R. M. What can the genome tell us about LDL cholesterol? Lancet 371, 450–452 (2008).
Lusis, A. J. & Pajukanta, P. A treasure trove for lipoprotein biology. Nature Genet. 40, 129–130 (2008).
Uyeda, K. & Repa, J. J. Carbohydrate response element binding protein, ChREBP, a transcription factor coupling hepatic glucose utilization and lipid synthesis. Cell. Metab. 4, 107–110 (2006).
Redon, R. et al. Global variation in copy number in the human genome. Nature 444, 444–454 (2006).
Pollex, R. L. & Hegele, R. A. Genomic copy number variation and its potential role in lipoprotein and metabolic phenotypes. Curr. Opin. Lipidol. 18, 174–180 (2007).
Reue, K. & Doolittle, M. H. Naturally occurring mutations in mice affecting lipid transport and metabolism. J. Lipid Res. 37, 1387–1405 (1996).
Beigneux, A. P. et al. Glycosylphosphatidylinositol-anchored high-density lipoprotein-binding protein 1 plays a critical role in the lipolytic processing of chylomicrons. Cell. Metab. 5, 279–291 (2007).
Gin, P. et al. Normal binding of lipoprotein lipase, chylomicrons, and apo-AV to GPIHBP1 containing a G56R amino acid substitution. Biochim. Biophys. Acta 1771, 1464–1468 (2007).
Wolfrum, C., Poy, M. N. & Stoffel, M. Apolipoprotein M is required for prebeta-HDL formation and cholesterol efflux to HDL and protects against atherosclerosis. Nature Med. 11, 418–422 (2005).
Shimizugawa, T. et al. ANGPTL3 decreases very low density lipoprotein triglyceride clearance by inhibition of lipoprotein lipase. J. Biol. Chem. 277, 33742–33748 (2002).
Koster, A. et al. Transgenic angiopoietin-like (angptl)4 overexpression and targeted disruption of angptl4 and angptl3: regulation of triglyceride metabolism. Endocrinology 146, 4943–4950 (2005).
Lee, M. H. et al. Identification of a gene, ABCG5, important in the regulation of dietary cholesterol absorption. Nature Genet. 27, 79–83 (2001).
Berge, K. E. et al. Accumulation of dietary cholesterol in sitosterolemia caused by mutations in adjacent ABC transporters. Science 290, 1771–1775 (2000).
Yang, C. et al. Disruption of cholesterol homeostasis by plant sterols. J. Clin. Invest. 114, 813–822 (2004).
Altmann, S. W. et al. Niemann-Pick C1 Like 1 protein is critical for intestinal cholesterol absorption. Science 303, 1201–1204 (2004).
Simon, J. S. et al. Sequence variation in NPC1L1 and association with improved LDL-cholesterol lowering in response to ezetimibe treatment. Genomics 86, 648–56 (2005).
Haemmerle, G. et al. Defective lipolysis and altered energy metabolism in mice lacking adipose triglyceride lipase. Science 312, 734–737 (2006).
Lass, A. et al. Adipose triglyceride lipase-mediated lipolysis of cellular fat stores is activated by CGI-58 and defective in Chanarin–Dorfman Syndrome. Cell. Metab. 3, 309–319 (2006).
Reue, K. The role of lipin 1 in adipogenesis and lipid metabolism. Novartis Found. Symp. 286, 58–68; discussion 68–71, 162–163, 196–203 (2007).
Brasaemle, D. L. Thematic review series: adipocyte biology. The perilipin family of structural lipid droplet proteins: stabilization of lipid droplets and control of lipolysis. J. Lipid Res. 48, 2547–2559 (2007).
Katan, M. B. Apolipoprotein E isoforms, serum cholesterol, and cancer. Lancet 1, 507–508 (1986).
Ebrahim, S. & Davey Smith, G. Mendelian randomization: can genetic epidemiology help redress the failures of observational epidemiology? Hum. Genet. 123, 15–33 (2008).
Cohen, J. C., Boerwinkle, E., Mosley, T. H. Jr & Hobbs, H. H. Sequence variations in PCSK9, low LDL, and protection against coronary heart disease. N. Engl. J. Med. 354, 1264–1272 (2006). An important study showing how Mendelian randomization can statistically connect genetic variants to the clinical end points that are mediated through plasma lipoproteins.
Baigent, C. et al. Efficacy and safety of cholesterol-lowering treatment: prospective meta-analysis of data from 90,056 participants in 14 randomised trials of statins. Lancet 366, 1267–1278 (2005).
Brown, M. S. & Goldstein, J. L. Biomedicine. Lowering LDL — not only how low, but how long? Science 311, 1721–1723 (2006).
Frikke-Schmidt, R. et al. Association of loss-of-function mutations in the ABCA1 gene with high-density lipoprotein cholesterol levels and risk of ischemic heart disease. JAMA 299, 2524–2532 (2008).
Ahnstrom, J. et al. Levels of apolipoprotein M are not associated with the risk of coronary heart disease in two independent case–control studies. J. Lipid Res. 49, 1912–1917 (2008).
Lusis, A. J. A thematic review series: systems biology approaches to metabolic and cardiovascular disorders. J. Lipid Res. 47, 1887–1890 (2006).
Goring, H. H. et al. Discovery of expression QTLs using large-scale transcriptional profiling in human lymphocytes. Nature Genet. 39, 1208–1216 (2007).
Chen, Y. et al. Variations in DNA elucidate molecular networks that cause disease. Nature 452, 429–435 (2008).
Reich, D. E. & Lander, E. S. On the allelic spectrum of human disease. Trends Genet. 17, 502–510 (2001).
Wang, W. Y., Barratt, B. J., Clayton, D. G. & Todd, J. A. Genome-wide association studies: theoretical and practical concerns. Nature Rev. Genet. 6, 109–118 (2005).
Wang, J. et al. Polygenic determinants of severe hypertriglyceridemia. Hum. Mol. Genet. 17, 2894–2899 (2008).
Steinberg, D., Glass, C. K. & Witztum, J. L. Evidence mandating earlier and more aggressive treatment of hypercholesterolemia. Circulation 118, 672–677 (2008).
Kathiresan, S. et al. Polymorphisms associated with cholesterol and risk of cardiovascular events. N. Engl. J. Med. 358, 1240–1249 (2008).
Humphries, S. E., Yiannakouris, N. & Talmud, P. J. Cardiovascular disease risk prediction using genetic information (gene scores): is it really informative? Curr. Opin. Lipidol. 19, 128–132 (2008).
Medina, M. W., Gao, F., Ruan, W., Rotter, J. I. & Krauss, R. M. Alternative splicing of 3-hydroxy-3-methylglutaryl coenzyme A reductase is associated with plasma low-density lipoprotein cholesterol response to simvastatin. Circulation 118, 355–362 (2008).
Frank-Kamenetsky, M. et al. Therapeutic RNAi targeting PCSK9 acutely lowers plasma cholesterol in rodents and LDL cholesterol in nonhuman primates. Proc. Natl Acad. Sci. USA 105, 11915–11920 (2008).
Akdim, F., Stroes, E. S. & Kastelein, J. J. Antisense apolipoprotein B therapy: where do we stand? Curr. Opin. Lipidol. 18, 397–400 (2007).
Holleboom, A. G., Vergeer, M., Hovingh, G. K., Kastelein, J. J. & Kuivenhoven, J. A. The value of HDL genetics. Curr. Opin. Lipidol. 19, 385–394 (2008).
Wang, J. et al. APOA5 genetic variants are markers for classic hyperlipoproteinemia phenotypes and hypertriglyceridemia. Nature Clin. Pract. Cardiovasc. Med. 5, 730–737 (2008).
Pullinger, C. R. et al. An apolipoprotein A-V gene SNP is associated with marked hypertriglyceridemia among Asian-American patients. J. Lipid Res. 49, 1846–1854 (2008).
Grundy, S. M. & Denke, M. A. Dietary influences on serum lipids and lipoproteins. J. Lipid Res. 31, 1149–1172 (1990).
Ordovas, J. M. Pharmacogenetics of lipid diseases. Hum. Genomics 1, 111–125 (2004).
Pollin, T. I. et al. A null mutation in human APOC3 confers a favorable lipid profile and apparent cardioprotection. Science 322, 1702–1705 (2008).
The author wishes to acknowledge the contributions to this field of numerous colleagues whose work could not be cited owing to space constraints. M. Peterfy, P. Connelly, M. Lanktree, T. Joy, P. Lahiry, J. Robinson, M. Ban, J. Wang and H. Cao provided helpful comments. The author is supported by the Jacob J. Wolfe Distinguished Medical Research Chair; the Edith Schulich Vinet Canada Research Chair (Tier I) in Human Genetics; the Jean Davignon Award for Cardiovascular Research (Pfizer, Canada); and by operating grants from the Canadian Institutes for Health Research (MOP-13430, MOP-39533, MOP-39833), the Heart and Stroke Foundation of Ontario (PRG-5967, NA-6059, T-6018), the Ontario Research Fund, and by Genome Canada through the Ontario Genomics Institute.
A member of a diverse group of hydrophobic compounds with many biological functions, such as structural components of cell membranes, energy storage sources and intermediates in signalling pathways.
A molecular complex containing proteins (apolipoproteins) and lipids (cholesterol or TG), which allow the lipid component to be soluble in plasma. TG-carrying lipoproteins are CMs and VLDL, whereas cholesterol-carrying lipoproteins are LDL and HDL.
A group of biochemical disorders characterized by quantitative disturbances in plasma lipids and lipoproteins, usually defined by deviations from age- and sex-specific normal ranges. Dyslipidaemia is a risk factor for CVD, such as stroke or heart attack.
- Genome-wide association (GWA) study
A powerful experimental approach for gene mapping that uses SNP markers across the human genome to identify genetic regions that are statistically associated with quantitative or qualitative traits in samples of unrelated individuals.
The specific name for the protein component of a lipoprotein. There are at least 13 different apolipoproteins, which have a variety of roles, including as enzyme cofactors and receptor ligands.
The objective and systematic acquisition of high-quality phenotypic data (that is, deep phenotyping), allowing for phenotypic features to be analysed on a continuum together with molecular data, such as gene expression profiles or causative genomic mutations.
- Framingham Heart Study
A widely cited longitudinal study of CVD based in Framingham, Massachusetts, that began in 1948 with 5,209 adult subjects and is currently studying its third generation of participants. It has greatly improved our understanding of risk factors for heart disease.
Also known as phytosterolaemia, this extremely rare autosomal recessive disorder is characterized by intestinal hyperabsorption and decreased biliary excretion of dietary sterols leading to hypercholesterolaemia, lipid deposits in the skin and tendons (xanthomas), and accelerated CVD.
A lipid-lowering drug that is the first member of the cholesterol absorption inhibitor class, which targets NPC1L1 on intestinal epithelial cells and in hepatocytes. This stimulates expression of cell-surface LDL receptors, resulting in increased clearance of LDL from the bloodstream.
- Mendelian randomization
The random assignment of alleles from parents to offspring that occurs during gamete formation. It is the underlying concept of a method to genetically stratify individuals in a large population sample and then evaluate phenotypic differences based on a pre-specified genotype.
- Network analysis
A blanket term for a range of computational methods to analyse complex sets of gene expression or related data in order to develop models of functionality, such as gene regulatory network models.
- Receiver operating characteristic (ROC) curve
A graphical plot, based on signal detection theory, which plots sensitivity along the y axis and 1 − specificity along the x axis for a binary classifier system — such as a genetic test or indeed any clinical test. ROC curve analysis can help select optimal diagnostic models and is fundamental to cost versus benefit analysis of diagnostic decision making.
Occurs when a single gene influences multiple phenotypic traits.
The interaction between genes when the action of one gene is modified by one or more other genes, which are sometimes called modifier genes.
A member of the class of lipid-lowering drugs that are used to treat people who have, or are at risk of, CVD. By inhibiting HMGCR — a key enzyme in cholesterol synthesis — statins ultimately stimulate the expression of cell-surface LDL receptors, resulting in an increased clearance of LDL from the bloodstream.
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Hegele, R. Plasma lipoproteins: genetic influences and clinical implications. Nat Rev Genet 10, 109–121 (2009). https://doi.org/10.1038/nrg2481
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