Apolipoprotein B levels, APOB alleles, and risk of ischemic cardiovascular disease in the general population, a review

Benn, Marianne

doi:10.1016/j.atherosclerosis.2009.01.004

Cited by 100 publications

(76 citation statements)

References 81 publications

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“…Fractional catabolic rate (pools per day) of LDL after injection was calculated as described ( 24,27 ). Individuals with mutations in the LDLR gene (W23X, W66G, W556S) and APOB gene (R3500Q, R3531C, E4154K) affecting the fractional catabolic rate of LDL were excluded ( 25 ). Ten individuals with APOB mutations [R3611Q (n = 4), T2488T (n = 5), P2712L (n = 1)] with no known effects on the fractional catabolic rate of LDL were included ( 25 ).…”

Section: Subjectsmentioning

confidence: 99%

“…Individuals with mutations in the LDLR gene (W23X, W66G, W556S) and APOB gene (R3500Q, R3531C, E4154K) affecting the fractional catabolic rate of LDL were excluded ( 25 ). Ten individuals with APOB mutations [R3611Q (n = 4), T2488T (n = 5), P2712L (n = 1)] with no known effects on the fractional catabolic rate of LDL were included ( 25 ). Samples taken prior to injection of labeled LDL (2002LDL ( -2005 were stored at -80°C and used for measurement of apoM ( 7 ).…”

Section: Subjectsmentioning

confidence: 99%

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The plasma concentration of HDL-associated apoM is influenced by LDL receptor-mediated clearance of apoB-containing particles

Christoffersen

Benn

Christensen

et al. 2012

Journal of Lipid Research

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This article is available online at http://www.jlr.org Supplementary key words lipoprotein • low-density lipoprotein metabolism • apolipoprotein • familial hypercholesterolemia HDL-associated apoM was recently shown to be a physiological carrier of sphingosine-1-phosphate (S1P) ( 1 ). S1P affects vascular integrity, and the S1P-dependent effects of HDL are dependent on apoM. Moreover, several studies have suggested that apoM can accelerate effl ux of cholesterol from foam cells, delay oxidation of LDL, and increase production of pre-␤ -HDL, suggesting that apoM affects antiatherogenic functions of HDL ( 2-4 ). However, little is known about the plasma metabolism of apoM. ApoM is anchored in HDL via a retained hydrophobic signal peptide ( 5 ). Loss of the signal peptide abolishes apoM's binding to HDL, causing rapid clearance of the truncated apoM in the kidney. Even though >90% of plasma apoM resides in HDL plasma, apoM concentration has consistently been shown to be positively correlated with plasma LDL cholesterol in humans ( 6-8 ). Moreover, HDL-associated plasma apoM is increased 2-fold in Ldlr Ϫ / Ϫ mice lacking functional LDL receptors ( 9 ). These observations might refl ect that plasma apoM is controlled by the rate of LDL receptor-mediated clearance of apoBcontaining particles. LDL receptor binding and internalization of LDL represent a major pathway controlling plasma LDL levels ( 10, 11 ), and the ligand binding domain of the LDL receptor, as well as the LDL receptor binding domain in apoB, have been extensively characterized ( 12, 13 ). The clinical diagnosis of familial hypercholesterolemia (FH) and impaired clearance of LDL can be caused by mutations in the LDLR and APOB genes ( 14 ). Genetic studies Abstract ApoM is mainly associated with HDL. Nevertheless, we have consistently observed positive correlations of apoM with plasma LDL cholesterol in humans. Moreover, LDL receptor defi ciency is associated with increased plasma apoM in mice. Here, we tested the idea that plasma apoM concentrations are affected by the rate of LDL receptormediated clearance of apoB-containing particles. We measured apoM in humans each carrying one of three different LDL receptor mutations (n = 9) or the apoB3500 mutation (n = 12). These carriers had increased plasma apoM (1.34 ± 0.13 µM, P = 0.003, and 1.23 ± 0.10 µM, P = 0.02, respectively) as compared with noncarriers (0.93 ± 0.04 µM). When we injected human apoM-containing HDL into Wt (n = 6) or LDL receptor-defi cient mice (n = 6), the removal of HDLassociated human apoM was delayed in the LDL receptordefi cient mice. After 2 h, 54 ± 5% versus 90 ± 8% ( P < 0.005) of the initial amounts of human apoM remained in the plasma of Wt and LDL receptor-defi cient mice, respectively. Finally, we compared the turnover of radio-iodinated LDL and plasma apoM concentrations in 45 normocholesterolemic humans. There was a negative correlation between plasma apoM and the fractional catabolic rate of LDL ( r = ؊ 0.38, P = 0.009). These data suggest that the plasma clearance of apoM...

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Section: Subjectsmentioning

confidence: 99%

Section: Subjectsmentioning

confidence: 99%

The plasma concentration of HDL-associated apoM is influenced by LDL receptor-mediated clearance of apoB-containing particles

Christoffersen

Benn

Christensen

et al. 2012

Journal of Lipid Research

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“…Elevated ApoB levels are associated with higher atherosclerotic plaque burden [2,3] and increased ApoB/ ApoA1 ratio is attributed to 49% of ACS events globally. Recently, evidence emerged that ApoB is a significant predictor for future cardiovascular events despite adequate LDL-C levels in patients with stable coronary disease [4][5][6].…”

Section: Introductionmentioning

confidence: 99%

Can Apolipoproteins apoB and apoB/apoA1 Ratio Predict Future Cardiovascular Risk Post Acute Coronary Syndrome? A Retrospective Cohort Study

Desplantie¹,

Ramanathan²

2016

J Clin Exp Cardiolog

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“…The apoB gene is located on chromosome 2 and comprises 29 exons. 1 Numerous studies have focused on the correlation between the apoB gene polymorphism and CHD risk. However, these studies result in conflicting conclusions.…”

Section: Introductionmentioning

confidence: 99%

Association between apolipoprotein B gene polymorphisms and the risk of coronary heart disease (CHD): an update meta-analysis

Zhang

Zheng

Yang

et al. 2015

J Renin Angiotensin Aldosterone Syst

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Objective: Polymorphisms in the apolipoprotein B (apoB) gene have been reported to be associated with coronary heart disease (CHD). However, the results on this topic are conflicting. The present study aims to derive a more precise estimation of the relationship between CHD and apoB genetic polymorphisms by meta-analysis. Methods:We identified a total of 54 studies involving 7236, 10,912, and 14,102 individuals, respectively, for EcoRI, XbaI, and SpIns/Del polymorphisms by searching in PubMed, Web of Science, Google Scholar, the Cochrane Library, Wanfang Data, SinoMed, and CNKI. We utilized RevMan 5.0 software to perform the meta-analyses. Results: A significant statistical association between apoB EcoRI polymorphism and CHD was observed under an allelic (p = 0.001, odds ratio (OR) = 1.33, 95% confidence interval (CI) = 1.12-1.57), dominant (p = 0.005, OR = 1.22, 95% CI = 1.06-1.40), and recessive (p = 0.04, OR = 1.33, 95% CI = 1.01-1.74) model. We also found similar association of apoB SpIns/Del polymorphism with CHD. However, we did not find association between apoB XbaI polymorphism and CHD. Conclusion:The current meta-analysis found an association of EcoRI polymorphism and SpIns/Del polymorphism with an increased risk of CHD. No significant association between apoB XbaI polymorphism and CHD we observed in the present study.

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Apolipoprotein B levels, APOB alleles, and risk of ischemic cardiovascular disease in the general population, a review

Cited by 100 publications

References 81 publications

The plasma concentration of HDL-associated apoM is influenced by LDL receptor-mediated clearance of apoB-containing particles

The plasma concentration of HDL-associated apoM is influenced by LDL receptor-mediated clearance of apoB-containing particles

Can Apolipoproteins apoB and apoB/apoA1 Ratio Predict Future Cardiovascular Risk Post Acute Coronary Syndrome? A Retrospective Cohort Study

Association between apolipoprotein B gene polymorphisms and the risk of coronary heart disease (CHD): an update meta-analysis

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