Fig. 3.

Model of cardiomyocyte remodeling and dedifferentiation during cardiac regeneration and repair. Activation of oncostatin M (OSM) induces dedifferentiation and hibernation in surviving cardiomyocytes. Dedifferentiation might be reversed after revascularization and hypertrophic stimulation. Invading macrophages remove debris and release OSM in the damaged heart. Cardiomyocytes dedifferentiate in response to OSM and re-establish cell–cell contacts. Hypertrophic signals (IGF-1) induce re-differentiation and hypertrophy of cardiomyocytes. Extended presence of dedifferentiation signals compromises contractility and promotes adverse myocardial remodeling