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• W2170767070 abstract "HomeArteriosclerosis, Thrombosis, and Vascular BiologyVol. 23, No. 10Genetics of Increased HDL Cholesterol Levels Free AccessEditorialPDF/EPUBAboutView PDFView EPUBSections ToolsAdd to favoritesDownload citationsTrack citationsPermissions ShareShare onFacebookTwitterLinked InMendeleyReddit Jump toFree AccessEditorialPDF/EPUBGenetics of Increased HDL Cholesterol LevelsInsights Into the Relationship Between HDL Metabolism and Atherosclerosis Marina Cuchel and Daniel J. Rader Marina CuchelMarina Cuchel From the University of Pennsylvania School of Medicine, Department of Medicine and Center for Experimental Therapeutics. Philadelphia, Pa. Search for more papers by this author and Daniel J. RaderDaniel J. Rader From the University of Pennsylvania School of Medicine, Department of Medicine and Center for Experimental Therapeutics. Philadelphia, Pa. Search for more papers by this author Originally published1 Oct 2003https://doi.org/10.1161/01.ATV.0000092947.15939.93Arteriosclerosis, Thrombosis, and Vascular Biology. 2003;23:1710–1712Astrong inverse association exists between plasma HDL cholesterol (HDL-C) levels and incidence of coronary artery disease.1 Although environmental factors play a role, variation in HDL-C levels are at least 50% genetically determined.2 The genetics of syndromes of very low HDL-C have been extensively studied. Mutations in apoA-I (the major HDL structural protein), ABCA1 (which promotes efflux of cellular lipids to apoA-I forming nascent HDL particles), and LCAT (which converts unesterified cholesterol to cholesteryl ester [CE] to form the lipid core of mature HDL particles) have all been demonstrated to cause very low levels of HDL-C and apoA-I due to rapid catabolism of apoA-I.3 However, their relationship to premature atherosclerosis is often uncertain, leading to the concept that the HDL-mediated “flux” of cholesterol from the periphery to the liver, where cholesterol is delivered for excretion into the bile (a process known as reverse cholesterol transport [RCT]), may be more important than the actual plasma concentrations of HDL-C in protecting against atherosclerosis.See page 1869Syndromes of inherited high HDL-C also exist, but have been much less studied. The only known monogenic cause of inherited high HDL-C in humans is deficiency of the cholesteryl ester transfer protein (CETP), which transfers HDL CE out of HDL to apoB-containing lipoproteins. CETP deficiency results in markedly reduced rates of turnover of apoA-I.4 CETP deficiency occurs primarily in Japan, where its relationship to cardiovascular risk is still under debate: some investigators believe it is associated with protection from cardiovascular disease,5 whereas others contend that it increases cardiovascular risk.6,7 This topic is not merely academic, as inhibitors of CETP are under development as novel HDL-raising therapies.8 Studies with CETP inhibitors will definitively answer whether raising HDL-C through CETP inhibition in humans reduces atherosclerotic vascular disease. The evolution of the CETP story—from the discovery of the deficiency state in humans to the development of therapeutics targeted toward CETP—has been a fascinating example of the ability of human genetic studies to enlighten our understanding of physiological pathways and lead to new therapies.Outside Japan, most subjects with inherited high HDL-C do not have CETP deficiency, and the genetic etiology of their high HDL-C is unknown. The only other gene in which genetic variation has been associated with elevated HDL-C levels in humans is hepatic lipase (HL). Patients deficient in HL have modestly increased HDL-C levels9 and a common variant in the HL promoter is associated with higher HDL-C levels.10 Patients with HL deficiency also have dyslipidemia and may be at increased risk of atherosclerotic vascular disease; thus, HL is not generally considered a viable target for pharmacologic inhibition. Genetic variations of another member of the lipase gene family, endothelial lipase (EL), might be also associated with elevated HDL-C levels. Overexpression of EL markedly reduces HDL-C levels,11 and antibody inhibition12 or deletion13,14 of EL significantly increases HDL-levels in mice. Several potentially functional genetic variants in EL were found in subjects with elevated HDL-C levels, some of which were not found in a large group of control subjects.15 One of these common EL variants was reported to be associated with slightly higher HDL-C levels.14 These studies have increased interest in EL as a potential target for pharmacologic intervention, although its relationship to atherosclerosis remains unknown. Further studies will elucidate whether mutations in EL are a monogenic cause of inherited high HDL-C and whether genetic variation in EL contributes to variation in HDL-C levels and atherosclerosis in the general population.Finally, scavenger receptor class B type I (SR-BI) is another candidate gene in which loss-of-function might be expected to result in high HDL-C levels. SR-BI was initially described by Acton and colleagues16 as a cell-surface receptor capable of binding HDL and mediating selective uptake of HDL CE into cells. In vivo studies have clearly demonstrated the crucial role of SR-BI in HDL metabolism and atherosclerosis in mice. Hepatic overexpression of SR-BI markedly reduced HDL-C levels17 and, paradoxically, reduced atherosclerosis in LDLR-deficient mice fed a high-cholesterol diet.18 Conversely, total or partial deficiency of SR-BI in mice causes increased HDL-C levels19,20 and accelerated atherosclerosis.21,22,23 These studies have led to the concept that hepatic SR-BI expression, by promoting the uptake of HDL CE, promotes RCT and therefore reduces atherosclerosis (Figure). However, direct measures of RCT from tissue to bile or feces have not been reported in SR-BI overexpressing or knockout mice and therefore this hypothesis remains to be tested. Furthermore, the effect of SR-BI on atherosclerosis is mediated not only by its hepatic expression, but also by its expression in other cell types that are involved in atherosclerosis. SR-BI is present in macrophages, where it mediates cholesterol efflux to mature HDL particles.24 Indeed, SR-BI deficiency is associated with increased lipid deposition in macrophages in vivo25 and bone marrow transplantation from SR-BI–deficient mice into LDLR-deficient mice resulted in increased atherosclerosis,26 consistent with an important role of macrophage SR-BI in protecting against atherosclerosis. Furthermore, endothelial SR-BI is required for the ability of HDL to stimulate endothelial eNOS expression and promote NO production.27 Tissue-specific SR-BI knockout mice will be required to definitively assess the effects of SR-BI in different tissues on HDL metabolism and especially atherogenesis. Download figureDownload PowerPointHDL metabolism and RCT. Lipid-poor apoA-I promotes efflux of cellular free cholesterol via the ABCA1 transporter. Mature HDL can also promote efflux of cellular free cholesterol via SR-BI. HDL free cholesterol can be esterified by LCAT to CE. HDL CE and FC are selectively taken up by the liver via SR-BI. HDL CE can also be transferred to apoB-containing lipoproteins via CETP. Mature HDL can be remodeled to smaller HDL particles through the action of hepatic lipase (hydrolysis of HDL triglycerides) and endothelial lipase (hydrolysis of HDL phospholipids). BA indicates bile acids; FC, free cholesterol; VLDL, very low density lipoprotein; LDLR, LDL receptor; HL, hepatic lipase.Whether SR-BI has similar role in HDL metabolism and atherogenesis in humans remains to be demonstrated. Surprisingly, SR-BI–deficient humans have not been described to date. Only three common polymorphisms have been reported that may be associated with LDL-C, HDL-C, and anthropometric measures in a sex-specific manner.28 Importantly, in this issue of Arteriosclerosis, Thrombosis, and Vascular Biology, Hsu et al29 report that a loss-of-function genetic variant in the human SR-BI gene is associated with increased plasma HDL-C levels. The investigators screened a Taiwanese Chinese population for mutations in the SR-BI promoter region and identified two novel variants. One (a single nucleotide polymorphism) was not associated with variation in HDL-C levels. The other (a promoter deletion of a putative binding site for the transcription factor SP1) was found in 2% of the population and was associated with significantly higher HDL-C levels. Reporter studies indicated that it has 30% less transcriptional activity in HepG2 cells, indicating the functional nature of this variant. Although the apparent effect of this SR-BI variant on HDL-C levels must be confirmed in other populations, this study provides important genetic evidence that SR-BI plays a role in HDL metabolism in humans.Major questions regarding the genetics of SR-BI and their relationship to atherosclerotic vascular disease in humans remain. For example, why have SR-BI–deficient subjects eluded the grasp of investigators to date? The phenotype of the SR-BI knockout mouse suggests that SR-BI deficiency in humans would be expected to cause elevated HDL-C levels in the setting of premature atherosclerotic disease, a phenotype that has been observed in humans. However, care must be taken when extrapolating from mouse models to humans with regard to HDL metabolism. Mice lack CETP, a state which could accentuate the phenotype of SR-BI deficiency. In the absence of CETP, HDL CE is dependent on the SR-BI pathway for clearance from the plasma, and disruption of the SR-BI pathway may constipate the RCT pathway, leading to accelerated atherosclerosis. Could it be that in humans, who have an intact CETP pathway, deficiency of hepatic SR-BI may have less consequence because HDL CE can be effectively siphoned from HDL and returned to the liver via apoB-containing lipoproteins? If true, the phenotype of SR-BI deficiency in humans may be more subtle than in the mouse. This may have potential therapeutic implications, in that persons with functional SR-BI mutations may not be good candidates for CETP inhibition. Another potential explanation for the failure to find SR-BI–deficient humans could be related to the role of SR-BI in reproduction. SR-BI is highly expressed in the gonads and SR-BI–deficient female mice are infertile.21,30 Perhaps loss-of-function mutations in SR-BI impair fertility in humans, markedly diminishing the chances of generating homozygotes with complete SR-BI deficiency.31The most fascinating aspect of the SR-BI–deficient phenotype in mice is the accelerated atherosclerosis. This would seem to be one of the strongest arguments that the RCT pathway is crucial to protection from atherosclerosis, at least in mice. Based on this result, one might predict that genetically reduced SR-BI function in humans would promote atherosclerosis despite the elevated HDL-C levels. Subsequent studies on the association of loss-of-function variants of SR-BI, such as the promoter variant described by Hsu and colleagues,29 with measures of atherosclerosis are eagerly awaited. If reduced SR-BI function is found to increase atherosclerosis in humans, it stands to reason that upregulation of SR-BI might be a novel anti-atherogenic strategy. The development of such a therapeutic approach, though firmly based in biology, would be complicated by the reduced plasma HDL-C levels.In summary, while the epidemiology indicates a strong inverse association between HDL-C and cardiovascular risk, at both extremes of the HDL-C distribution, genetic conditions that influence HDL metabolism have a far less predictable relationship to atherosclerosis. Studies of genetic causes of very low HDL-C have provided important insight into the physiology of HDL metabolism and identified new molecular targets for the development of new therapies targeted toward HDL. As in the case of CETP, ongoing studies of genetic causes of very high HDL-C also promise to provide similarly important insights on the complex relationship between HDL metabolism and atherosclerosis that could lead to new therapies for the treatment of atherosclerotic cardiovascular disease.MC is supported by a K12 award from the National Institutes of Health (RR17625). DJR is an Established Investigator of the American Heart Association, a recipient of the Burroughs Wellcome Foundation Clinical Scientist Award in Translational Research, and a recipient of a Doris Duke Distinguished Clinical Scientist Award.FootnotesCorrespondence to Daniel J. Rader, MD, University of Pennsylvania School of Medicine, 654 BRBII/III Labs, 421 Curie Blvd, Philadelphia, PA 19104. E-mail [email protected] References 1 Gordon DJ, Rifkind BM. High-density lipoproteins: the clinical implications of recent studies. 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Hepatic lipase deficiency. Crit Rev Clin Lab Sci. 1998; 35: 547–572.CrossrefMedlineGoogle Scholar10 Cohen JC, Vega GL, Grundy SM. Hepatic lipase: new insights from genetic and metabolic studies. Curr Opin Lipidol. 1999; 10: 259–267.CrossrefMedlineGoogle Scholar11 Jaye M, Lynch KJ, Krawiec J, Marchadier D, Maugeais C, Doan K, South V, Amin D, Perrone M, Rader DJ. A novel endothelial-derived lipase that modulates HDL metabolism. Nat Genet. 1999; 21: 424–428.CrossrefMedlineGoogle Scholar12 Jin W, Millar JS, Broedl U, Glick JM, Rader DJ. Inhibition of endothelial lipase causes increased HDL cholesterol levels in vivo. J Clin Invest. 2003; 111: 357–362.CrossrefMedlineGoogle Scholar13 Ishida T, Choi S, Kundu RK, Hirata K, Rubin EM, Cooper AD, Quertermous T. Endothelial lipase is a major determinant of HDL level. J Clin Invest. 2003; 111: 347–355.CrossrefMedlineGoogle Scholar14 Ma K, Cilingiroglu M, Otvos JD, Ballantyne CM, Marian AJ, Chan L. Endothelial lipase is a major genetic determinant for high-density lipoprotein concentration, structure, and metabolism. Proc Natl Acad Sci U S A. 2003; 100: 2748–2753.CrossrefMedlineGoogle Scholar15 deLemos AS, Wolfe ML, Long CJ, Sivapackianathan R, Rader DJ. Identification of genetic variants in endothelial lipase in persons with elevated high-density lipoprotein cholesterol. Circulation. 2002; 106: 1321–1326.LinkGoogle Scholar16 Acton S, Rigotti A, Landschultz KT, Xu S, Hobbs HH, Krieger M. Identification of scavenger receptor SR-BI as a high density lipoprotein receptor. Science. 1996; 271: 518–520.CrossrefMedlineGoogle Scholar17 Kozarsky KF, Donahee MH, Rigotti A, Iqbal SN, Edelman ER, Krieger M. Overexpression of the HDL receptor SR-BI alter plasma HDL and bile cholesterol levels. Nature. 1997; 387: 414–417.CrossrefMedlineGoogle Scholar18 Kozarsky KF, Donahee MH, Glick JM, Krieger M, Rader DJ. Gene transfer and hepatic overexpression of the HDL receptor SR-BI reduces atherosclerosis in the cholesterol-fed LDL receptor deficient mouse. Arterioscler Thromb Vasc Biol. 2000; 20: 721–727.CrossrefMedlineGoogle Scholar19 Rigotti A, Trigatti BL, Penman M, Rayburn H, Herz J, Krieger M. A targeted mutation in the murine gene encoding the high density lipoprotein (HDL) receptor scavenger receptor class B type I reveals role in HDL metabolism. Proc Natl Acad Sci U S A. 1997; 94: 12610–12615.CrossrefMedlineGoogle Scholar20 Varban ML, Rinninger F, Wang N, Fairchild-Huntress V, Dunmore JH, Fang Q, Gosselin ML, Dixon KL, Deeds JD, Acton SL, Tall AR. Targeted mutation reveals a central role for SR-BI in hepatic selective uptake of high density lipoprotein cholesterol. Proc Natl Acad Sci U S A. 1998; 95: 4619–4624.CrossrefMedlineGoogle Scholar21 Trigatti B, Rayburn H, Vinals M, Braun A, Mettienen H, Penman M, Hertz M, Schrenzel M, Amigo L, Rigotti A, Krieger M. Influence of the high density lipoprotein receptor SR-BI on reproductive and cardiovascular pathophysiology. Proc Natl Acad Sci U S A. 1999; 96: 9322–9327.CrossrefMedlineGoogle Scholar22 Huszar D, Verban ML, Rinninger F, Feeley R, Arai T, Fairchild-Huntress V, Donovan MJ, Tall AR. Increased LDL cholesterol and atherosclerosis in LDL receptor-deficient mice with attenuated expression of scavenger receptor BI. Arterioscler Thromb Vasc Biol. 2000; 20: 1068–1073.CrossrefMedlineGoogle Scholar23 Braun A, Trigatti BL, Post MJ, Sato K, Simons M, Edelberg JM, Rosenberg RD, Schrenzel M, Krieger M. Loss of SR-BI expression leads to the early onset of occlusive atherosclerotic coronary artery disease, spontaneous myocardial infarctions, severe cardiac dysfunction, and premature death in apolipoprotein E-deficient mice. Circ Res. 2002; 90: 270–276.CrossrefMedlineGoogle Scholar24 Rothblat GH, de la Llera-Moya M, Atger V, Kellner-Weibel G, Williams DL, Phillips MC. 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Scavenger receptor class B type I is a multiligand HDL receptor that influences diverse physiologic systems. J Clin Invest. 2001; 108: 793–797.CrossrefMedlineGoogle Scholar Previous Back to top Next FiguresReferencesRelatedDetailsCited By Rayat S, Ramezanidoraki N, Kazemi N, Modarressi M, Falah M, Zardadi S and Morovvati S (2022) Association study between polymorphisms in MIA3, SELE, SMAD3 and CETP genes and coronary artery disease in an Iranian population, BMC Cardiovascular Disorders, 10.1186/s12872-022-02695-6, 22:1 Gong J, Asher S, Cucchiara B, Cuchel M and Soffer D (2021) Case report: 68 yo Chinese-American woman with high HDL-C and ischemic stroke attributed to intracranial atherosclerotic stenosis, Journal of Clinical Lipidology, 10.1016/j.jacl.2021.01.006, 15:2, (248-254), Online publication date: 1-Mar-2021. 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