Shinji Makino and colleagues have successfully isolated a cardiomyogenic cell line (CMG) from murine bone marrow stromal cells. The cells were immortalized using 5-azacytidine treatment, which induced spontaneous beating and morphological changes. These cells expressed atrial natriuretic peptide and brain natriuretic peptide, and stained positively for myosin, desmin, and actinin. Electron microscopy revealed a cardiomyocyte-like ultrastructure, including typical sarcomeres, a centrally positioned nucleus, and atrial granules. The CMG cells exhibited various action potentials, including sinus node-like and ventricular cell-like potentials, with long action potential durations, shallow resting membrane potentials, and pacemaker-like late diastolic slow depolarization. The expression of cardiomyocyte-specific genes, such as Nkx2.5/Csx, GATA4, TEF-1, and MEF-2C, was observed before and after 5-azacytidine treatment. This new cell line provides a valuable model for studying cardiomyocyte differentiation and gene therapy strategies for heart disease.Shinji Makino and colleagues have successfully isolated a cardiomyogenic cell line (CMG) from murine bone marrow stromal cells. The cells were immortalized using 5-azacytidine treatment, which induced spontaneous beating and morphological changes. These cells expressed atrial natriuretic peptide and brain natriuretic peptide, and stained positively for myosin, desmin, and actinin. Electron microscopy revealed a cardiomyocyte-like ultrastructure, including typical sarcomeres, a centrally positioned nucleus, and atrial granules. The CMG cells exhibited various action potentials, including sinus node-like and ventricular cell-like potentials, with long action potential durations, shallow resting membrane potentials, and pacemaker-like late diastolic slow depolarization. The expression of cardiomyocyte-specific genes, such as Nkx2.5/Csx, GATA4, TEF-1, and MEF-2C, was observed before and after 5-azacytidine treatment. This new cell line provides a valuable model for studying cardiomyocyte differentiation and gene therapy strategies for heart disease.