ArticleAtherosclerosis2017
Identifying low density lipoprotein cholesterol associated variants in the Annexin A2 (ANXA2) gene.
Article in Atherosclerosis, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 21 citations in OpenAlex.
- Identification and evaluation of a lipid-lowering small compound as a PCSK9 inhibitor.Journal of advanced research · 2026Article
- A Pilot Study ofBalkan journal of medical genetics : BJMG · 2024Article
- The lncRNA GAS5 upregulates ANXA2 to mediate the macrophage inflammatory response during atherosclerosis development.Heliyon · 2024Article
- Tale of two systems: the intertwining duality of fibrinolysis and lipoprotein metabolism.Journal of thrombosis and haemostasis : JTH · 2023Review
- Translational implications of targeting annexin A2: From membrane repair to muscular dystrophy, cardiovascular disease and cancer.Clinical and translational discovery · 2023Article
- Emerging Insights on the Diverse Roles of Proprotein Convertase Subtilisin/Kexin Type 9 (PCSK9) in Chronic Liver Diseases: Cholesterol Metabolism and Beyond.International journal of molecular sciences · 2022Review
- Annexins and cardiovascular diseases: Beyond membrane trafficking and repair.Frontiers in cell and developmental biology · 2022Review
- Article
- Annexin Animal Models-From Fundamental Principles to Translational Research.International journal of molecular sciences · 2021Review
- Multi-Omics Integrative Analysis Uncovers Molecular Subtypes and mRNAs as Therapeutic Targets for Liver Cancer.Frontiers in medicine · 2021Article
- [Serum annexin A2 level is significantly elevated in patients with coronary heart disease].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2020Article
- Article
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Authors and funding
24 authors at 10 institutions in 5 countries.
Funding
Abstract
BACKGROUND AND
aimsAnnexin-A2 (AnxA2) is an endogenous inhibitor of proprotein convertase subtilisin/kexin type-9 (PCSK9). The repeat-one (R1) domain of AnxA2 binds to PCSK9, blocking its ability to promote degradation of low-density lipoprotein cholesterol-receptors (LDL-R) and thereby regulate low-density lipoprotein cholesterol (LDL-C) levels. Here we identify variants in ANXA2 influencing LDL-C levels and we determine the molecular mechanisms of their effects.
resultsThe ANXA2 single nucleotide polymorphism (SNP) genotype-phenotype association was examined using the Second-Northwick-Park Heart Study (NPHSII) (n∼2700) and the UCL-LSHTM-Edinburgh-Bristol (UCLEB) consortium (n∼14,600). The ANXA2-R1 domain coding-SNP rs17845226 (V98L) associated with LDL-C, homozygotes for the minor allele having ≈18.8% higher levels of LDL-C (p = 0.004), and higher risk of coronary heart disease (CHD) (p = 0.04). The SNP is in modest linkage disequilibrium (r
conclusionsBoth rs11633032 and rs17191344 SNPs are functional variants, where the minor alleles create repressor-binding protein sites for transcription factors that contribute to reduced ANXA2 gene expression. Lower AnxA2 levels could increase plasma levels of PCSK9 and thus increase LDL-C levels and risk of CHD. This supports, for the first time in humans, previous observations in mouse models that changes in the levels of AnxA2 directly influence plasma LDL-C levels, and thus implicate this protein as a potential therapeutic target for LDL-C lowering.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.