{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"omics_type":["Unknown"],"volume":["8(9)"],"submitter":["Luo M"],"pubmed_abstract":["<h4>Background and aims</h4>Several observational studies have reported inconsistent associations between dyslipidaemia, stains use and atopic dermatitis (AD). Nevertheless, the available data on the effects of -C-lowering as well as TG-lowering drugs remain inconclusive and limited. The aim of this study was to evaluate the causal association of lipid traits and long-term use of lipid-lowering drugs on AD risk.<h4>Methods</h4>Drug-targeted Mendelian randomization analyses were performed in European ancestry. Pooled statistics on low-density lipoprotein cholesterol, triglyceride and AD were extracted from large genome-wide association studies datasets. Instrumental variables located in and around lipid-lowering target genes were used as proxies for therapeutic inhibition of these target genes. Inverse-variance-weighted approach was applied as the primary analysis.<h4>Results</h4>We explored the role of seven lipid-lowering target genes in AD, among which genetically proxied Niemann-Pick C1-like 1 inhibition, a target of LDL-C-lowering drugs, was associated with an increased risk of AD (odds ratio, 3.03; 95% CI, 1.36-6.75; <i>p</i> = 0.007). This association was replicated in FinnGen cohort (odds ratio, 1.72; 95% CI, 1.09-2.72; <i>p</i> = 0.020). A series of sensitivity analyses confirmed the robustness of the estimates.<h4>Conclusion</h4>We found no genetic support for the repurposing of seven lipid-lowering drug targets for the prevention of AD. However, pharmacovigilance of AD risk in Niemann-Pick C1-like 1 inhibitor users may be warranted."],"journal":["Health science reports"],"pagination":["e71040"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC12415263"],"repository":["biostudies-literature"],"pubmed_title":["Genetic Association of Lipids and Lipid-Lowering Drug Target Genes With Atopic Dermatitis: A Drug Target Mendelian Randomization Study."],"pmcid":["PMC12415263"],"pubmed_authors":["Luo M","Han Y","Lin J","Zhuo Q","Lin L"],"additional_accession":[]},"is_claimable":false,"name":"Genetic Association of Lipids and Lipid-Lowering Drug Target Genes With Atopic Dermatitis: A Drug Target Mendelian Randomization Study.","description":"<h4>Background and aims</h4>Several observational studies have reported inconsistent associations between dyslipidaemia, stains use and atopic dermatitis (AD). Nevertheless, the available data on the effects of -C-lowering as well as TG-lowering drugs remain inconclusive and limited. The aim of this study was to evaluate the causal association of lipid traits and long-term use of lipid-lowering drugs on AD risk.<h4>Methods</h4>Drug-targeted Mendelian randomization analyses were performed in European ancestry. Pooled statistics on low-density lipoprotein cholesterol, triglyceride and AD were extracted from large genome-wide association studies datasets. Instrumental variables located in and around lipid-lowering target genes were used as proxies for therapeutic inhibition of these target genes. Inverse-variance-weighted approach was applied as the primary analysis.<h4>Results</h4>We explored the role of seven lipid-lowering target genes in AD, among which genetically proxied Niemann-Pick C1-like 1 inhibition, a target of LDL-C-lowering drugs, was associated with an increased risk of AD (odds ratio, 3.03; 95% CI, 1.36-6.75; <i>p</i> = 0.007). This association was replicated in FinnGen cohort (odds ratio, 1.72; 95% CI, 1.09-2.72; <i>p</i> = 0.020). A series of sensitivity analyses confirmed the robustness of the estimates.<h4>Conclusion</h4>We found no genetic support for the repurposing of seven lipid-lowering drug targets for the prevention of AD. However, pharmacovigilance of AD risk in Niemann-Pick C1-like 1 inhibitor users may be warranted.","dates":{"release":"2025-01-01T00:00:00Z","publication":"2025 Sep","modification":"2026-06-02T02:44:37.856Z","creation":"2026-04-13T03:12:47.143Z"},"accession":"S-EPMC12415263","cross_references":{"pubmed":["40927812"],"doi":["10.1002/hsr2.71040"]}}