Association of cholesteryl ester transfer protein (CETP) gene polymorphism, high density lipoprotein cholesterol and risk of coronary artery disease: a meta-analysis using a Mendelian randomization approach
Open accessAbstract
BACKGROUND: Recent randomized controlled trials have challenged the concept that increased high density lipoprotein cholesterol (HDL-C) levels are associated with coronary artery disease (CAD) risk reduction. The causal role of HDL-C in the development of atherosclerosis remains unclear. To increase precision and to minimize residual confounding, we exploited the cholesteryl ester transfer protein (CETP)-TaqIB polymorphism as an instrument based on Mendelian randomization. METHODS: The Mendelian randomization analysis was performed by two steps. First, we conducted a meta-analysis of 47 studies, including 23,928 cases and 27,068 controls, to quantify the relationship between the TaqIB polymorphism and the CAD risk. Next, the association between the TaqIB polymorphism and HDL-C was assessed among 5,929 Caucasians. We further employed Mendelian randomization to evaluate the causal effect of HDL-C on CAD based on the findings from the meta-analysis. RESULTS: The overall comparison of the B2 allele with the B1 allele yielded a significant risk reduction of CAD (P < 0.0001; OR = 0.88; 95% CI: 0.84-0.92) with substantial between-study heterogeneity (I² = 55.2%; P(heterogeneity) <0.0001). The result was not materially changed after excluding the Hardy-Weinberg Equilibrium (HWE)-violation studies. Compared with B1B1 homozygotes, Caucasian carriers of the B2 allele had a 0.25 mmol/L increase in HDL-C level (95% CI: 0.20-0.31; P <0.0001; I² = 0; P(heterogeneity) =0.87). However, a 1 standard deviation (SD) elevation in HDL-C levels due to the TaqIB polymorphism, was marginal associated with CAD risk (OR =0.79; 95% CI: 0.54-1.03; P =0.08). CONCLUSIONS: Taken together, our results lend support to the concept that increased HDL-C cannot be translated into a reduction in CAD risk.
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Large Mendelian randomisation studies indicate that increased HDL-cholesterol cannot be translated into a reduction in CVD risk.
“Further, large Mendelian randomisation studies indicate that increased HDLcholesterol cannot be translated into a reduction in CVD risk (42,43)”
From Effects of low-carbohydrate diets<i>v</i>. low-fat diets on body weight and cardiovascular risk factors: a meta-analysis of randomised controlled trials (2016) · cites this paper as [43]
The Abstract Conclusions state that increased HDL-C cannot be translated into reduced coronary artery disease (CAD) risk. The Conclusion limits the Mendelian-randomization inference to CAD among Caucasians; the citing sentence broadens this to cardiovascular disease (CVD) risk generally. (LLM, conf=0.85)
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“CAD was regarded as the main outcome in most of the studies [11,17,21,22,36-40,42,44,45,47,49-51,53,5561,64-66], except 8 studies analyzed MI [20,43,46,48, 52,54,62,63] and 2 studies analyzed ACS [41] as the endpoint.”
InfluentialEck, M. V., Ye, D., Hildebrand, R. B., Kruijt, J. K., de Haan, W., Hoekstra, M., Rensen, P. C. N., Ehnholm, C., Jauhiainen, M., & van Berkel, T. J. C. (2007) · Circulation Research · doi:10.1161/01.res.0000260202.79927.4f · Cited by 46 · cited 1× · see citing works
“Whether CETP efforts pro- or anti-atherogenic effects, by means of the LDL-C receptor pathway, is still unclear [80,81].”
Whiting, B. M., Anderson, J. L., Muhlestein, J. B., Horne, B. D., Bair, T. L., Pearson, R. R., & Carlquist, J. F. (2005) · American Heart Journal · doi:10.1016/j.ahj.2004.08.034 · Cited by 44 · cited 12× · see citing works
“CAD was regarded as the main outcome in most of the studies [11,17,21,22,36-40,42,44,45,47,49-51,53,5561,64-66], except 8 studies analyzed MI [20,43,46,48, 52,54,62,63] and 2 studies analyzed ACS [41] as the endpoint.”
InfluentialDurlach, A., Clavel, C., Girard-Globa, A., & Durlach, V. (1999) · The Journal of Clinical Endocrinology & Metabolism · doi:10.1210/jcem.84.10.6064 · Cited by 43 · cited 10× · see citing works
“CAD was regarded as the main outcome in most of the studies [11,17,21,22,36-40,42,44,45,47,49-51,53,5561,64-66], except 8 studies analyzed MI [20,43,46,48, 52,54,62,63] and 2 studies analyzed ACS [41] as the endpoint.”
InfluentialSchierer, A., Been, L. F., Ralhan, S. K., Wander, G. S., Aston, C. E., & Sanghera, D. K. (2011) · Pharmacogenetics and Genomics · doi:10.1097/fpc.0b013e32834dc9ef · Cited by 43 · cited 11× · see citing works
“CAD was regarded as the main outcome in most of the studies [11,17,21,22,36-40,42,44,45,47,49-51,53,5561,64-66], except 8 studies analyzed MI [20,43,46,48, 52,54,62,63] and 2 studies analyzed ACS [41] as the endpoint.”
InfluentialArca, M., Montali, A., Ombres, D., Battiloro, E., Campagna, F., Ricci, G., & Verna, R. (2001) · Clinical Genetics · doi:10.1034/j.1399-0004.2001.600510.x · Cited by 41 · cited 11× · see citing works
“CAD was regarded as the main outcome in most of the studies [11,17,21,22,36-40,42,44,45,47,49-51,53,5561,64-66], except 8 studies analyzed MI [20,43,46,48, 52,54,62,63] and 2 studies analyzed ACS [41] as the endpoint.”
InfluentialCastle, W. E. (1903) · Science · doi:10.1126/science.18.456.396 · Cited by 41 · cited 1× · see citing works
“The logic of this approach is greatly strengthened by the appeal to Mendelian randomization [24], which is according to Mendel’s second law (the law of independent assortment) [25].”
Ziegler, A., Pahlke, F., & König, I. R. (2008) · Statistics in Medicine · doi:10.1002/sim.3213 · Cited by 39 · see citing works
McCaskie, P. A., Beilby, J. P., Chapman, C., Hung, J., McQuillan, B., Thompson, P. L., & Palmer, L. J. (2007) · Human Genetics · doi:10.1007/s00439-007-0326-2 · Cited by 38 · cited 11× · see citing works
“CAD was regarded as the main outcome in most of the studies [11,17,21,22,36-40,42,44,45,47,49-51,53,5561,64-66], except 8 studies analyzed MI [20,43,46,48, 52,54,62,63] and 2 studies analyzed ACS [41] as the endpoint.”
InfluentialShah, S. H., Casas, J. P., Gaunt, T. R., Cooper, J. A., Drenos, F., Zabaneh, D., Swerdlow, D. I., Shah, T., Sofat, R., Palmen, J., et al. (2012) · European Heart Journal · doi:10.1093/eurheartj/ehs243 · Cited by 38 · cited 1× · see citing works
“Observational and experimental studies have documented a strong positive association of low density lipoprotein cholesterol (LDL-C) and an inverse association of high density lipoprotein cholesterol (HDL-C) with the risk of CAD [2].”
Kawasaki, I., Tahara, H., Emoto, M., Shoji, T., & Nishizawà, Y. (2002) · Diabetes · doi:10.2337/diabetes.51.3.871 · Cited by 37 · cited 10× · see citing works
“CAD was regarded as the main outcome in most of the studies [11,17,21,22,36-40,42,44,45,47,49-51,53,5561,64-66], except 8 studies analyzed MI [20,43,46,48, 52,54,62,63] and 2 studies analyzed ACS [41] as the endpoint.”
InfluentialYılmaz, H., sbir, T., Ağaçhan, B., & Karaali, Z. (2004) · Cell Biochemistry and Function · doi:10.1002/cbf.1124 · Cited by 37 · cited 11× · see citing works
“CAD was regarded as the main outcome in most of the studies [11,17,21,22,36-40,42,44,45,47,49-51,53,5561,64-66], except 8 studies analyzed MI [20,43,46,48, 52,54,62,63] and 2 studies analyzed ACS [41] as the endpoint.”
InfluentialGenetic variants associated with VLDL, LDL and HDL particle size differ with race/ethnicity
Wood, A. C., Manichaikul, A. W., Aslibekyan, S. W., Borecki, I. B., Goff, D. C., Hopkins, P. N., Lai, C., Ordovás, J. M., Post, W. S., Rich, S. S., et al. (2012) · Human Genetics · doi:10.1007/s00439-012-1256-1 · Cited by 34 · cited 1× · see citing works
“Given some GWASs have identified that numerous lipid-associated genetic variations differ with ethnicity [72-74], we expect that future investigations of the TaqIB polymorphism will uncover its genetic ancestral backgrounds and pleiotropic effects.”
Park, K., Choi, J., Kim, H., Oh, S., Chae, I., Kim, H. S., Oh, B., Lee, M. M., Yb, P., & Choi, Y. (2002) · Clinical Genetics · doi:10.1034/j.1399-0004.2003.630105.x · Cited by 31 · cited 10× · see citing works
“CAD was regarded as the main outcome in most of the studies [11,17,21,22,36-40,42,44,45,47,49-51,53,5561,64-66], except 8 studies analyzed MI [20,43,46,48, 52,54,62,63] and 2 studies analyzed ACS [41] as the endpoint.”
InfluentialPrevalence of genetic risk factors for coronary artery disease in Corsica island (France)
Falchi, A., Giovannoni, L., Piras, I. S., Calò, C. M., Moral, P., Vona, G., & Varesi, L. (2005) · Experimental and Molecular Pathology · doi:10.1016/j.yexmp.2005.09.005 · Cited by 29 · cited 10× · see citing works
“CAD was regarded as the main outcome in most of the studies [11,17,21,22,36-40,42,44,45,47,49-51,53,5561,64-66], except 8 studies analyzed MI [20,43,46,48, 52,54,62,63] and 2 studies analyzed ACS [41] as the endpoint.”
InfluentialAdjusting for covariates in logistic regression models
Xing, G., & Xing, C. (2010) · Genetic Epidemiology · doi:10.1002/gepi.20526 · Cited by 26 · cited 1× · see citing works
“To test the reliability and robustness of our data, we did a statistical power analysis as previously described [68,69].”
Corella, D., Carrasco, P., Amiano, P., Arriola, L., Chirlaque, M. D., Huerta, J. M., Martínez, C., Martínez‐Camblor, P., Molina‐Montes, E., Navarro, C., et al. (2010) · Atherosclerosis · doi:10.1016/j.atherosclerosis.2010.03.026 · Cited by 25 · cited 11× · see citing works
“CAD was regarded as the main outcome in most of the studies [11,17,21,22,36-40,42,44,45,47,49-51,53,5561,64-66], except 8 studies analyzed MI [20,43,46,48, 52,54,62,63] and 2 studies analyzed ACS [41] as the endpoint.”
InfluentialResnick, H. E., Rodríguez, B. L., Havlik, R. J., Ferrucci, L., Foley, D. J., Curb, J. D., & Harris, T. B. (2000) · Genetic Epidemiology · doi:10.1002/1098-2272(200007)19:1 · Cited by 25 · see citing works
Muendlein, A., Saely, C. H., Marte, T., Schmid, F. M., Koch, L., Rein, P., Langer, P. H., Aczél, S., & Drexel, H. (2008) · Atherosclerosis · doi:10.1016/j.atherosclerosis.2007.10.030 · Cited by 25 · cited 4× · see citing works
“in Asian subjects [11,38,47,51,57,58,60,63,65,66], 26 in Caucasian subjects [17,20-22,36,37,40-46,49,50,52-56, 59,61,62,64,67] and one mixed- population study [48].”
InfluentialAssociation of lipoprotein lipase D9N polymorphism with myocardial infarction in type 2 diabetes
Izar, M. C. D. O., Helfenstein, T., Ihara, S. S. M., Relvas, W. G. M., dos Santos, A. O., Fischer, S. C. M., Pinto, L. E. S. A., Lopes, I. E. L., Pomaro, D. R., Fonseca, M. I. H., et al. (2008) · Atherosclerosis · doi:10.1016/j.atherosclerosis.2008.08.006 · Cited by 24 · cited 11× · see citing works
“CAD was regarded as the main outcome in most of the studies [11,17,21,22,36-40,42,44,45,47,49-51,53,5561,64-66], except 8 studies analyzed MI [20,43,46,48, 52,54,62,63] and 2 studies analyzed ACS [41] as the endpoint.”
InfluentialPadmaja, N., Kumar, R., Balachander, J., & Adithan, C. (2009) · Clinica Chimica Acta · doi:10.1016/j.cca.2008.12.041 · Cited by 24 · cited 4× · see citing works
“in Asian subjects [11,38,47,51,57,58,60,63,65,66], 26 in Caucasian subjects [17,20-22,36,37,40-46,49,50,52-56, 59,61,62,64,67] and one mixed- population study [48].”
InfluentialMeiner, V., Friedlander, Y., Milo, H., Sharon, N. A., Avi, L. B., Shpitzen, S., Leitersdorf, E., Siscovick, D. S., & Schwartz, S. M. (2008) · Annals of Human Genetics · doi:10.1111/j.1469-1809.2008.00464.x · Cited by 24 · cited 10× · see citing works
“CAD was regarded as the main outcome in most of the studies [11,17,21,22,36-40,42,44,45,47,49-51,53,5561,64-66], except 8 studies analyzed MI [20,43,46,48, 52,54,62,63] and 2 studies analyzed ACS [41] as the endpoint.”
InfluentialPoduri, A., Khullar, M., Bahl, A., Sharma, Y. P., & Talwar, K. K. (2009) · DNA and Cell Biology · doi:10.1089/dna.2009.0887 · Cited by 22 · cited 10× · see citing works
“In addition, the magnitude of association was greater in H-B studies than in P-B studies; the OR is likely overestimated, since subjects sampled from a single hospital may not reflect the real environmental exposures in the source population.”
InfluentialKolovou, G. D., Vasiliadis, I. K., Kolovou, V., Karakosta, A., Mavrogeni, S. I., Papadopoulou, E., Papamentzelopoulos, S., Giannakopoulou, V., Marvaki, A., Degiannis, D., et al. (2011) · Lipids in Health and Disease · doi:10.1186/1476-511x-10-156 · Cited by 21 · cited 10× · see citing works
“CAD was regarded as the main outcome in most of the studies [11,17,21,22,36-40,42,44,45,47,49-51,53,5561,64-66], except 8 studies analyzed MI [20,43,46,48, 52,54,62,63] and 2 studies analyzed ACS [41] as the endpoint.”
InfluentialWu, Z., Lou, Y., Jin, W., Liu, Y., Lu, L., & Lü, G. (2012) · Molecular Biology Reports · doi:10.1007/s11033-012-2384-3 · Cited by 21 · see citing works
Self-citationRejeb, J., Omezzine, A., Rebhi, L., Naffeti, I., Kchok, K., Belkahla, R., HadjMbarek, I. B., Rejeb, N. B., Nabli, N., Boujelbene, A., et al. (2008) · Archives of cardiovascular diseases · doi:10.1016/j.acvd.2008.09.013 · Cited by 20 · cited 9× · see citing works
“In addition, the magnitude of association was greater in H-B studies than in P-B studies; the OR is likely overestimated, since subjects sampled from a single hospital may not reflect the real environmental exposures in the source population.”
InfluentialHorne, B. D., Camp, N. J., Anderson, J. L., Mower, C. P., Clarke, J., Kolek, M. J., & Carlquist, J. F. (2007) · Journal of the American College of Cardiology · doi:10.1016/j.jacc.2007.02.039 · Cited by 20 · cited 11× · see citing works
“CAD was regarded as the main outcome in most of the studies [11,17,21,22,36-40,42,44,45,47,49-51,53,5561,64-66], except 8 studies analyzed MI [20,43,46,48, 52,54,62,63] and 2 studies analyzed ACS [41] as the endpoint.”
InfluentialDedoussis, G. V., Panagiotakos, D. B., Louizou, E., Mantoglou, I., Chrysohoou, C. A., Lamnissou, K., Pitsavos, C. E., & Stefanadis, C. (2007) · Human Heredity · doi:10.1159/000099827 · Cited by 20 · cited 17× · see citing works
“CAD was regarded as the main outcome in most of the studies [11,17,21,22,36-40,42,44,45,47,49-51,53,5561,64-66], except 8 studies analyzed MI [20,43,46,48, 52,54,62,63] and 2 studies analyzed ACS [41] as the endpoint.”
InfluentialRahimi, Z., Norouzirad, R., Vaisi‐Raygani, A., Saidi, M. R., Rahimi, Z., Ahmadi, R., Yarani, R., Hamzehee, K., & Parsian, A. (2011) · Genetic Testing and Molecular Biomarkers · doi:10.1089/gtmb.2011.0037 · Cited by 20 · cited 10× · see citing works
“In addition, the magnitude of association was greater in H-B studies than in P-B studies; the OR is likely overestimated, since subjects sampled from a single hospital may not reflect the real environmental exposures in the source population.”
InfluentialBhanushali, A. A., & Das, B. R. (2010) · Journal of Community Genetics · doi:10.1007/s12687-010-0005-1 · Cited by 19 · cited 10× · see citing works
“CAD was regarded as the main outcome in most of the studies [11,17,21,22,36-40,42,44,45,47,49-51,53,5561,64-66], except 8 studies analyzed MI [20,43,46,48, 52,54,62,63] and 2 studies analyzed ACS [41] as the endpoint.”
InfluentialThe CETP TaqIB Polymorphism Is Associated With the Risk of Sudden Death in Type 2 Diabetic Patients
Porchay-Baldérelli, I., Péan, F., Bellili-Muñoz, N., Jaziri, R., Marre, M., Fumeron, F., & for the DIABHYCAR Study Group (2007) · Diabetes Care · doi:10.2337/dc07-0869 · Cited by 19 · see citing works
Zheng, K.-Q., Zhang, S., He, Y., Zhang, L., Zhang, K., Huang, D., & Sun, Y. (2004) · PubMed · Cited by 19 · see citing works
Hsieh, M., Tien, K., Chang, S., Lo, C., Hsin, S., Hsiao, J., Hsu, S.-C., Liang, H., Chen, H., Shin, S., et al. (2007) · Metabolism · doi:10.1016/j.metabol.2006.12.023 · Cited by 17 · cited 10× · see citing works
“CAD was regarded as the main outcome in most of the studies [11,17,21,22,36-40,42,44,45,47,49-51,53,5561,64-66], except 8 studies analyzed MI [20,43,46,48, 52,54,62,63] and 2 studies analyzed ACS [41] as the endpoint.”
InfluentialAtherosclerosis in aged mice over-expressing the reverse cholesterol transport genes
Berti, J. A., de Faria, E. C., & Oliveira, H. C. F. (2005) · Brazilian Journal of Medical and Biological Research · doi:10.1590/s0100-879x2005000300010 · Cited by 11 · cited 2× · see citing works
“However, another in vivo study reported that CETP expression reduced atherosclerosis in lecithin cholesterol acyltransferase (LCAT) transgenic mice [85] and a further study revealed that CETP offset the deleterious effect of LCAT [86].”
Blankenberg, S., Tiret, L., Bickel, C., Schlitt, A., Jungmair, W., Genth‐Zotz, S., Lubos, E., Espinola–Klein, C., & Hj, R. (2004) · PubMed · doi:10.1007/s00392-004-1404-2 · Cited by 11 · cited 9× · see citing works
“CAD was regarded as the main outcome in most of the studies [11,17,21,22,36-40,42,44,45,47,49-51,53,5561,64-66], except 8 studies analyzed MI [20,43,46,48, 52,54,62,63] and 2 studies analyzed ACS [41] as the endpoint.”
InfluentialKaestner, S., Πατσούρας, Ν., Spathas, D. H., Flordellis, C. S., & Manolis, A. S. (2009) · Angiology · doi:10.1177/0003319709348297 · Cited by 8 · cited 10× · see citing works
“CAD was regarded as the main outcome in most of the studies [11,17,21,22,36-40,42,44,45,47,49-51,53,5561,64-66], except 8 studies analyzed MI [20,43,46,48, 52,54,62,63] and 2 studies analyzed ACS [41] as the endpoint.”
InfluentialHigh HDL may not protect the heart. Concentrate on lowering LDL for now, experts advise.
(2012) · PubMed · Cited by 1 · see citing works
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Mansoor, N., Vinknes, K. J., Veierød, M. B., & Retterstøl, K. (2016) · British Journal of Nutrition · doi:10.1017/s0007114515004699 · Cited by 439 · see citing works
“Further, large Mendelian randomisation studies indicate that increased HDLcholesterol cannot be translated into a reduction in CVD risk((42,43)).”
BackgroundLipid-Lowering Agents: Targets Beyond PCSK9
Hegele, R. A., & Tsimikas, S. (2019) · Circulation Research · doi:10.1161/circresaha.118.313171 · Cited by 171 · see citing works
“ASCVD risk,(204) whereas other studies showed either a marginal increase in ASCVD risk despite favorable HDL-C levels(187) or no change in ASCVD risk.(205) The contradictory genetic findings were paralleled by inconsistent RCT experience with small-molecule inhibitors of CETP.”
ResultHDL and atherosclerotic cardiovascular disease: genetic insights into complex biology
Rosenson, R. S., Brewer, H. B., Barter, P. J., Björkegren, J., Chapman, M. J., Gaudet, D., Kim, D. S., Niesor, E. J., Rye, K., Sacks, F. M., et al. (2017) · Nature Reviews Cardiology · doi:10.1038/nrcardio.2017.115 · Cited by 148 · see citing works
Update on the molecular biology of dyslipidemias
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HDL Cholesterol Metabolism and the Risk of CHD: New Insights from Human Genetics
Vitali, C., Khetarpal, S. A., & Rader, D. J. (2017) · Current Cardiology Reports · doi:10.1007/s11886-017-0940-0 · Cited by 94 · see citing works
The Role of High-Density Lipoproteins in Diabetes and Its Vascular Complications
Wong, N. K. P., Nicholls, S. J., Tan, J. T. M., & Bursill, C. A. (2018) · International Journal of Molecular Sciences · doi:10.3390/ijms19061680 · Cited by 77 · see citing works
“Some studies have found that genetically lower CETP concentrations and lower CETP activity associated with this polymorphism can lead to a lower risk of CAD [38,39], while other studies have not replicated this [40].”
Byrkjeland, R., Stensæth, K.-H., Anderssen, S. A., Njerve, I. U., Arnesen, H., Seljeflot, I., & Solheim, S. (2016) · Cardiovascular Diabetology · doi:10.1186/s12933-016-0336-2 · Cited by 71 · see citing works
Present therapeutic role of cholesteryl ester transfer protein inhibitors
Ferri, N., Corsini, A., Sirtori, C. R., & Ruscica, M. (2017) · Pharmacological Research · doi:10.1016/j.phrs.2017.12.028 · Cited by 56 · see citing works
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“The absence of a causal link between HDL-C and CAD was also confirmed by Mendelian randomization studies; indeed, individuals with genetic polymorphisms associated with high levels of HDL-C did not show any improvement in cardiovascular health [23,24].”
BackgroundJonas, K., & Kopeć, G. (2019) · International Journal of Molecular Sciences · doi:10.3390/ijms20143514 · Cited by 31 · see citing works
“The recent meta-analysis with the Mendelian randomization approach also showed that increased HDL associated with CETP gene polymorphism cannot be translated into reduction of cardiovascular risk [19].”
MethodEyvazian, V. A., & Frishman, W. H. (2017) · Cardiology in Review · doi:10.1097/crd.0000000000000137 · Cited by 29 · see citing works
Mendelian randomization studies on atherosclerotic cardiovascular disease: evidence and limitations
Hu, Q., Hao, P., Liu, Q., Dong, M., Gong, Y., Zhang, C., & Zhang, Y. (2019) · Science China Life Sciences · doi:10.1007/s11427-019-9537-4 · Cited by 30 · see citing works
Naerr, G. W., Rein, P., Saely, C., & Drexel, H. (2016) · Vascular pharmacology · doi:10.1016/j.vph.2016.01.006 · Cited by 31 · see citing works
Hyperalphalipoproteinemia and Beyond: The Role of HDL in Cardiovascular Diseases
Giammanco, A., Noto, D., Barbagallo, C. M., Nardi, E., Caldarella, R., Ciaccio, M., Averna, M. R., & Cefalu, A. B. (2021) · Life · doi:10.3390/life11060581 · Cited by 26 · see citing works
Xu, S., Cheng, J., Li, N., Chen, Y.-N., Cai, M., Tang, S.-S., Huang, H., Zhang, B., Cen, J.-M., Yang, X.-L., et al. (2015) · Lipids in Health and Disease · doi:10.1186/s12944-015-0065-7 · Cited by 18 · see citing works
“Accumulating evidences have suggested that SNPs within the lipid metabolism-related genes might potentially contribute to CAD [24–27].”
BackgroundCholesteryl ester transfer protein inhibitors in precision medicine
Su, X., Li, G., Deng, Y., & Chang, D. (2020) · Clinica Chimica Acta · doi:10.1016/j.cca.2020.09.012 · Cited by 14 · see citing works
Christen, T., Trompet, S., Noordam, R., Blauw, L. L., Gast, K. B., Rensen, P. C. N., van Dijk, K. W., Rosendaal, F. R., de Mutsert, R., & Jukema, J. W. (2017) · Journal of clinical lipidology · doi:10.1016/j.jacl.2017.10.023 · Cited by 12 · see citing works
Siri, S. R. A., Eliassen, B. M., Jacobsen, B. K., Melhus, M., Broderstad, A. R., Michalsen, V. L., & Braaten, T. (2019) · BMJ Open · doi:10.1136/bmjopen-2019-028939 · Cited by 12 · see citing works
Liu, X., Harding, S., & Rideout, T. (2022) · Current Atherosclerosis Reports · doi:10.1007/s11883-022-01014-w · Cited by 9 · see citing works
Yang, R., Wu, S., Zhao, Z., Deng, X., Deng, Q.-Y., Wang, D., & Liu, Q. (2024) · Clinical Research in Cardiology · doi:10.1007/s00392-024-02420-7 · Cited by 8 · see citing works
“Although prospective cohort studies and thorough experimental research provide evidence for low HDL as a biomarker risk of CAD [10], others have identified correlations that are weak or insignificant [21, 40].”
Genetics for the Identification of Lipid Targets Beyond PCSK9
Wang, L. R., & Hegele, R. A. (2016) · Canadian Journal of Cardiology · doi:10.1016/j.cjca.2016.11.003 · Cited by 8 · see citing works
“More recently, Mendelian randomization studies in some populations suggested that carriers of common DNA variants in the CETP gene had increased HDL cholesterol and significantly decreased CVD risk (38), while other similar studies showed either a marginal increase in CVD risk despite favorable HDL cholesterol levels…”
Common variants associated with blood lipid levels do not affect carotid plaque composition
Siemelink, M. A., van der Laan, S. W., van Setten, J., de Vries, J. P. P. M., de Borst, G. J., Moll, F. L., den Ruijter, H. M., Asselbergs, F. W., Pasterkamp, G., & de Bakker, P. I. W. (2015) · Atherosclerosis · doi:10.1016/j.atherosclerosis.2015.07.041 · Cited by 8 · see citing works
“The notable exception is a negative association between HDL-C levels and the occurrence of composite cardiovascular endpoints, which may represent a non-causal effect (e.g. due to reverse causation or uncorrected confounding), consistent with recent Mendelian randomization studies [2,4,5].”
Cholesteryl ester transfer protein: ace of spades, queen of hearts, or the joker?
Miller, N. E. (2015) · Frontiers in Pharmacology · doi:10.3389/fphar.2015.00145 · Cited by 7 · see citing works
“Using Mendelian randomization, Wu et al. (2014) found the B2 allele to be associated with a lower risk of coronary heart disease (CHD).”
BackgroundLow-carbohydrate diets increase LDL-cholesterol, and thereby indicate increased risk of CVD
Mansoor, N., Vinknes, K. J., Veierød, M. B., & Retterstøl, K. (2016) · British Journal Of Nutrition · doi:10.1017/s0007114516001343 · Cited by 7 · see citing works
Biomarkers and Gene Polymorphisms in Members of Long- and Short-lived Families: A Longevity Study
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“Both TaqIB and I405V variants are the most widely studied and were found to be associated with CAD [5, 14, 15], left main CAD [16] and longevity [17, 18].”
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The Role of Some LPL Gene Polymorphisms with Cardiovascular Disease
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- Authors
- Wu, Z., Lou, Y., Qiu, X., Liu, Y., Lu, L., Chen, Q., & Jin, W.
- Affiliations
- Shanghai Jiao Tong University (CN)
- Corresponding author
- Jin, Wei
- Venue
- BMC Medical Genetics
- Published
- 2014-10-23
- Volume
- 15
- Issue
- 1
- Pages
- 118-118
- ISSN
- 1471-2350 (ISSN-L)
- PMC
- PMC4258818
- OpenAlex
- W2027819554
- Cited by
- 40
- References
- 97
- Citations by year
- 2026: 1 · 2024: 1 · 2023: 2 · 2022: 1 · 2021: 2 · 2020: 1 · 2019: 6 · 2018: 3 · 2017: 7 · 2016: 7 · 2015: 8
- FWCI
- 0.97
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Locations
- BMC Medical Genetics (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- Funders
- Natural Science Foundation of Shanghai
- National Natural Science Foundation of China (81070177, 81370397)
- Science and Technology Commission of Shanghai Municipality (14YF1402700)
- Shanghai Municipal Health Bureau (XBR2013100)
- Beijing Municipal Science and Technology Commission
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Genetic Associations and Epidemiology
- Health Sciences › Medicine › Surgery › Lipoproteins and Cardiovascular Health
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Clinical Biochemistry › Paraoxonase enzyme and polymorphisms
- Keywords
- cholesteryl ester transfer protein, CETP gene polymorphisms, TaqIB polymorphism, HDL cholesterol, coronary artery disease, atherosclerosis, Mendelian randomization
- MeSH terms
- Alleles, Coronary Artery Disease, Homozygote, Humans, Cholesterol, HDL, Random Allocation, Risk Factors, Odds Ratio, Databases, Factual, Polymorphism, Single Nucleotide, Cholesterol Ester Transfer Proteins, Genetic Association Studies
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