Dr Mavroidis has studied the first desmin mutation identified in humans suffering from dilated cardiomyopathy and was the first to suggest an interplay between desmin’s head and tail domains (doi: 10.1096/fj.07-088724). Now days, there is an increasing number of reports indicating that desmin posttranslational modifications precede development of heart failure (HF), suggesting a key role for desmin as cardiomyocytes“stress sensor” in HF. Also our studies have shown that Inhibition of complement system improves cardiac function, fibrosis/remodeling, arrhythmias and survival after endurance training in an arrhythmogenic cardiomyopathy animal model (doi: 10.1007/s00395-015-0485-6; PMID: 33897891). This study was the first to implicate complement system activation in the progression of the disease. It was not until very recently, that the concept of an important role of inflammation and autoimmunity as new targets and paradigms in ACM management is emerged in the field.
