ArticlePharmacogenetics and genomics2014
The MYLIP p.N342S polymorphism is associated with response to lipid-lowering therapy in Brazilian patients with familial hypercholesterolemia.
Article in Pharmacogenetics and genomics, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers, 1 of them a synthesis that pooled it.
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Who cites it
8 citing papers in PubMed, 1 synthesis or guideline pooled it, 19 citations in OpenAlex.
- Ezetimibe for the prevention of cardiovascular disease and all-cause mortality events.The Cochrane database of systematic reviews · 2018 · on this mapPooled it
- IDOL N342S Variant, Atherosclerosis Progression and Cardiovascular Disorders in the Italian General Population.PloS one · 2015Trial
- Genome-wide identification and immunological expression analysis of the C3HC4-type zinc finger protein genes in the silkworm, Bombyx Mori.BMC genomics · 2026Article
- Precision Medicine in Cardiovascular Disease Prevention: Clinical Validation of Multi-Ancestry Polygenic Risk Scores in a U.S. Cohort.Nutrients · 2025Article
- Pharmacogenomics of statins: lipid response and other outcomes in Brazilian cohorts.Pharmacological reports : PR · 2022Review
- Idol Depletion Protects against Spontaneous Atherosclerosis in a Hamster Model of Familial Hypercholesterolemia.Oxidative medicine and cellular longevity · 2022Article
- Pharmacogenomics Variability of Lipid-Lowering Therapies in Familial Hypercholesterolemia.Journal of personalized medicine · 2021Review
- miR-19b promotes breast cancer metastasis through targeting MYLIP and its related cell adhesion molecules.Oncotarget · 2017Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundA previous study reported that the myosin regulatory light chain interacting protein (MYLIP) might serve as a novel therapeutic class for treating dyslipidemia. It contributes to variations in the levels of circulating low-density lipoprotein cholesterol (LDL-C), promoting the degradation of LDL-LDLR, thus limiting absorption. The effect of genetic variation in the MYLIP gene in a disease scenario characterized by mutations in the LDLR gene has not been previously evaluated.
objectiveThe aim of this study was to assess the effect of the p.N342S variant on the response to lipid-lowering therapy in Brazilian patients with heterozygous familial hypercholesterolemia (FH). PATIENTS AND
methodsA total of 156 patients with heterozygous FH were followed up for 12 months and received lipid-lowering therapy (different doses of atorvastatin with the addition of ezetimibe in over half the patients of each genotype group). Cholesterol data were assessed, and analysis of the MYLIP rs9370867 (p.N342S) genotypes was carried out by melting curve analysis.
resultsBaseline total cholesterol and baseline LDL-C levels were not different between genotypes. After 1 year of treatment, LDL-C responses (expressed as mg/dl and as %) were significantly different among genotypes (AA: -79±68 and -39±27, GA: -60±79 and -27±32, and GG: -30±83 and -15±38; P=0.02 and 0.005, respectively). In addition, FH patients carrying the AA genotype were more likely to achieve LDL-C levels of less than 130 mg/dl after 1 year of treatment (75.0%) compared with patients with the GG and GA genotypes (34.5 and 34.8%, respectively; P=0.001).
conclusionOur study indicates that MYLIP p.N342S might be a pharmacogenetic marker for lipid-lowering therapy in patients with FH.
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