By contrast, persistent or excessive OSM/OSMR activation drives maladaptive remodeling and heart failure; sustained OSM signaling is increased in dilated cardiomyopathy and diabetic cardiomyopathy, where it promotes cardiomyocyte dedifferentiation and contractile failure, while genetic or pharmacologic OSMRβ inhibition ameliorates inflammatory heart failure [43]. This evidence concerns the gene OSMR and diabetic cardiomyopathy.