{"title":"Bridging the inflammation gap by IL-6 inhibition","authors":"Michael D. Shapiro","doi":"10.1038/s44161-025-00702-5","DOIUrl":null,"url":null,"abstract":"Targeting inflammation has emerged as a promising strategy to reduce residual cardiovascular risk. A study now uses human genetics to show that IL-6 inhibition is associated with a lower risk of cardiovascular disease with no increase in infection, supporting the use of pharmacological treatments that target IL-6 rather than its receptor.","PeriodicalId":74245,"journal":{"name":"Nature cardiovascular research","volume":"4 9","pages":"1043-1044"},"PeriodicalIF":10.8000,"publicationDate":"2025-08-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Nature cardiovascular research","FirstCategoryId":"1085","ListUrlMain":"https://www.nature.com/articles/s44161-025-00702-5","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q1","JCRName":"CARDIAC & CARDIOVASCULAR SYSTEMS","Score":null,"Total":0}
引用次数: 0
Abstract
Targeting inflammation has emerged as a promising strategy to reduce residual cardiovascular risk. A study now uses human genetics to show that IL-6 inhibition is associated with a lower risk of cardiovascular disease with no increase in infection, supporting the use of pharmacological treatments that target IL-6 rather than its receptor.