{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Ciofani JL"],"funding":["British Heart Foundation","Medical Research Council"],"pagination":["18810"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC10620428"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["13(1)"],"pubmed_abstract":["There are currently no approved pharmacological treatment options for aortic stenosis (AS), and there are limited identified drug targets for this chronic condition. It remains unclear whether inflammation plays a role in AS pathogenesis and whether immunomodulation could become a therapeutic target. We evaluated the potentially causal association between inflammation and AS by investigating the genetically proxied effects of tocilizumab (IL6 receptor, IL6R, inhibitor), canakinumab (IL1β inhibitor) and colchicine (β-tubulin inhibitor) through a Mendelian randomisation (MR) approach. Genetic proxies for these drugs were identified as single nucleotide polymorphisms (SNPs) in the gene, enhancer or promoter regions of IL6R, IL1β or β-tubulin gene isoforms, respectively, that were significantl"],"journal":["Scientific reports"],"pubmed_title":["The effect of immunomodulatory drugs on aortic stenosis: a Mendelian randomisation analysis."],"pmcid":["PMC10620428"],"funding_grant_id":["FS/IPBSRF/22/27060","MC_UP_1201/21"],"pubmed_authors":["De Maria GL","Rahimi K","Banning AP","Allahwala UK","Han D","Bhindi R","Nazarzadeh M","Ciofani JL"],"additional_accession":[]},"is_claimable":false,"name":"The effect of immunomodulatory drugs on aortic stenosis: a Mendelian randomisation analysis.","description":"There are currently no approved pharmacological treatment options for aortic stenosis (AS), and there are limited identified drug targets for this chronic condition. It remains unclear whether inflammation plays a role in AS pathogenesis and whether immunomodulation could become a therapeutic target. We evaluated the potentially causal association between inflammation and AS by investigating the genetically proxied effects of tocilizumab (IL6 receptor, IL6R, inhibitor), canakinumab (IL1β inhibitor) and colchicine (β-tubulin inhibitor) through a Mendelian randomisation (MR) approach. Genetic proxies for these drugs were identified as single nucleotide polymorphisms (SNPs) in the gene, enhancer or promoter regions of IL6R, IL1β or β-tubulin gene isoforms, respectively, that were significantl","dates":{"release":"2023-01-01T00:00:00Z","publication":"2023 Nov","modification":"2026-05-28T08:34:21.765Z","creation":"2025-02-18T23:30:19.745Z"},"accession":"S-EPMC10620428","cross_references":{"pubmed":["37914784"],"doi":["10.1038/s41598-023-44387-x"]}}