ArticleAtherosclerosis2022
The effect of LPA Thr3888Pro on lipoprotein(a) and coronary artery disease is modified by the LPA KIV-2 variant 4925G>A.
Article in Atherosclerosis, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 25 citations in OpenAlex.
- Recent advances in understanding the spectrum of genetic determinants of lipoprotein(a) levels.Current opinion in lipidology · 2026Review
- A Position Paper on Lipoprotein(a) From the Lipoprotein(a) Task Force of the Korean Society of Lipid and Atherosclerosis: Current Evidence, Clinical Applications, and Future Directions.Korean circulation journal · 2026Review
- A Position Paper on Lipoprotein(a) From the Lipoprotein(a) Task Force of the Korean Society of Lipid and Atherosclerosis: Current Evidence, Clinical Applications, and Future Directions.Journal of lipid and atherosclerosis · 2026Review
- Resolving intra-repeat variation in medically relevant VNTRs from short-read sequencing data using the cardiovascular risk gene LPA as a model.Genome biology · 2024Article
- Assessment of Apolipoprotein(a) Isoform Size Using Phenotypic and Genotypic Methods.International journal of molecular sciences · 2023Review
- CORRESPONDENCE: MNOS3 RS1799983 AND RS2070744 POLYMORPHISMS AND CHRONIC KIDNEY DISEASE AND CORONARY HEART DISEASE IN POPULATION WITH TYPE 2 DIABETES.Acta endocrinologica (Bucharest, Romania : 2005)Article
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Authors and funding
12 authors at 3 institutions in 2 countries.
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Abstract
BACKGROUND AND
aimsHigh lipoprotein(a) [Lp(a)] concentrations are associated with increased coronary artery disease (CAD) risk. Lp(a) is regulated mainly genetically by the LPA gene but involved genetic variants have not been fully elucidated. Improved understanding of the entanglements of genetic Lp(a) regulation may enhance genetic prediction of Lp(a) and CAD risk. We investigated an interaction between the well-known LPA missense SNP rs41272110 (known as Thr3888Pro) and the frequent LPA splicing mutation KIV-2 4925G>A.
methodsEffects on Lp(a) concentrations were investigated by multiple quantile regression in the German Chronic Kidney Disease (GCKD) study, KORA-F3 and KORA-F4 (n
resultsWe observed a significant SNP-SNP interaction in all studies (p = 1.26e-05 to 3.03e-04). In quantile regression analysis, rs41272110 as a predictor shows no impact on Lp(a) (β = -0.06 [-0.79; 0.68], p = 0.879), but in a joint model including both SNPs as predictors, rs41272110 is associated with markedly higher Lp(a) (β = +9.40 mg/dL [6.45; 12.34], p = 4.07e-10). Similarly, rs41272110 shows no effect on CAD in UKB (HR = 1.01 [0.97; 1.04], p = 0.731), while rs41272110 carriers not carrying 4925G>A show an increased CAD risk (HR = 1.10 [1.04; 1.16], p = 6.9e-04). This group corresponds to 4% of the population. Adjustment for apolipoprotein(a) isoforms further modified the effect estimates markedly.
conclusionsThis work emphasizes the complexity of the genetic regulation of Lp(a) and the importance to account for genetic subgroups in Lp(a) association studies and when interpreting genetic cardiovascular risk profiles.
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