Cardiomyocytes continuously generate the contractile force to circulate blood 
through the body. Imbalances in contractile performance or energy supply cause 
adaptive responses of the heart resulting in adverse rearrangement of regular 
structures, which in turn might lead to heart failure. At the cellular level, 
cardiomyocyte remodeling includes (1) restructuring of the contractile 
apparatus; (2) rearrangement of the cytoskeleton; and (3) changes in energy 
metabolism. Dedifferentiation represents a key feature of cardiomyocyte 
remodeling. It is characterized by reciprocal changes in the expression pattern 
of "mature" and "immature" cardiomyocyte-specific genes. Dedifferentiation may 
enable cardiomyocytes to cope with hypoxic stress by disassembly of the energy 
demanding contractile machinery and by reduction of the cellular energy demand. 
Dedifferentiation during myocardial repair might provide cardiomyocytes with 
additional plasticity, enabling survival under hypoxic conditions and increasing 
the propensity to enter the cell cycle. Although dedifferentiation of 
cardiomyocytes has been described during tissue regeneration in zebrafish and 
newts, little is known about corresponding mechanisms and regulatory circuits in 
mammals. The recent finding that the cytokine oncostatin M (OSM) is pivotal for 
cardiomyocyte dedifferentiation and exerts strong protective effects during 
myocardial infarction highlights the role of cytokines as potent stimulators of 
cardiac remodeling. Here, we summarize the current knowledge about transient 
dedifferentiation of cardiomyocytes in the context of myocardial remodeling, and 
propose a model for the role of OSM in this process.