biostudies-literatureCiofani JLBritish Heart FoundationMedical Research Council18810https://www.ebi.ac.uk/biostudies/studies/S-EPMC10620428biostudies-literatureUnknown13(1)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 significantlScientific reportsThe effect of immunomodulatory drugs on aortic stenosis: a Mendelian randomisation analysis.PMC10620428FS/IPBSRF/22/27060MC_UP_1201/21De Maria GLRahimi KBanning APAllahwala UKHan DBhindi RNazarzadeh MCiofani JLfalseThe effect of immunomodulatory drugs on aortic stenosis: a Mendelian randomisation analysis.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 significantl2023-01-01T00:00:00Z2023 Nov2026-05-28T08:34:21.765Z2025-02-18T23:30:19.745ZS-EPMC106204283791478410.1038/s41598-023-44387-x