New Treatment Approach for Myocarditis: Boosting Cardiac Anti-inflammatory Abilities to Combat Viruses
Myocarditis is an inflammatory heart disease, most commonly caused by viral infections. Common symptoms of acute myocarditis include mild chest discomfort and palpitations after activity, while severe cases can lead to acute heart failure or even sudden death. Currently, researchers have limited understanding of the mechanisms behind myocarditis, and clinically, comprehensive treatment plans relying on life support are primarily used to allow the heart to rest and gradually recover its function. Now, the team led by Professor Wang Daowen proposes a new treatment approach that empowers the heart to “actively counterattack” against viruses by enhancing its anti-inflammatory abilities, aiming to alleviate myocardial inflammation reactions and cardiac functional damage.
New Treatment Approach for Myocarditis: Boosting Cardiac Anti-inflammatory Abilities to Combat Viruses
Professor Wang Daowen explains that arachidonic acid is an essential polyunsaturated fatty acid in the human body, and it holds significant importance in maintaining the structure and function of cell membranes. Previous studies have indicated that the metabolites of arachidonic acid, known as EETs (epoxyeicosatrienoic acids), possess strong biological activity and can exert specific anti-inflammatory protective functions in certain cells or locations. However, EETs are unstable and are quickly “digested” by soluble epoxide hydrolase (sEH). By using sEH inhibitors to suppress sEH activity and reduce EETs metabolism, it may be possible to enhance their biological functions, including anti-inflammatory effects.
Starting from a clinical perspective, Professor Wang Daowen’s team conducted liquid chromatography-tandem mass spectrometry analysis of clinical samples. They first revealed a significant decrease in EETs levels in the bodies of myocarditis patients, correlating with increased expression and activity of sEH. Similar findings were observed in an animal model of myocarditis induced by Coxsackievirus B3 (CVB3).
In further animal and cell mechanism studies, the team discovered that inhibiting sEH or externally applying EETs could increase EETs levels, enhance Type I interferon signaling, stimulate the production of Type I interferons, reduce CVB3 replication, and demonstrate antiviral effects. This, in turn, alleviated the cardiac functional damage caused by viral infections.
