Team identifies new targets to treat myocardial infarction
In a paper published Monday in Nature Medicine, researchers from Massachusetts General Hospital and colleagues identified the mechanism behind an elevated immune response after myocardial infarction and suggested interferon regulatory factor 3 (IRF3), interferon alpha/beta receptor 1 (IFNAR1) and cGAMP synthase (cGAS) could be new targets in mitigating potentially fatal damage caused by post-MI inflammation.
The researchers observed higher expression of IRF3 and IRF3-dependent cytokines in whole-infarct tissue as early as one day after MI in wild-type mice compared with mice without MI. Among the elevated cytokines were type I interferons including IFN beta (IFNB1), which can amplify inflammatory responses. In contrast, mice with IRF3 knockout showed almost no increase in type I IFN expression following MI, mirroring wild-type mice without MI...