Bone marrow cells (BMC) can repair infarcted hearts by differentiating into myocytes and vascular structures, improving heart function and survival. In a study, BMC were mobilized using stem cell factor (SCF) and granulocyte-colony stimulating factor (G-CSF), leading to significant tissue regeneration and reduced mortality in mice with myocardial infarction. The study showed that BMC home to the infarcted region, replicate, and differentiate into new myocytes and vascular structures, which connect to the unaffected ventricle. This process resulted in a 68% decrease in mortality, a 40% reduction in infarct size, and a 70% decrease in diastolic stress. The new myocytes and vessels improved ventricular function and reduced cavitary dilation. The study also demonstrated that BMC can transdifferentiate into cardiac cells, including endothelial cells and smooth muscle cells, and that this process is influenced by tissue damage and the presence of pluripotent cells. The findings suggest that cytokine-mediated mobilization of BMC could be a noninvasive therapeutic strategy for myocardial regeneration in ischemic heart disease and other cardiac conditions. The study highlights the potential of BMC as a source of cardiac repair and the importance of understanding the molecular mechanisms underlying their transdifferentiation. The results indicate that BMC can replace dead cardiac tissue and restore heart function, offering a promising approach for treating heart disease.Bone marrow cells (BMC) can repair infarcted hearts by differentiating into myocytes and vascular structures, improving heart function and survival. In a study, BMC were mobilized using stem cell factor (SCF) and granulocyte-colony stimulating factor (G-CSF), leading to significant tissue regeneration and reduced mortality in mice with myocardial infarction. The study showed that BMC home to the infarcted region, replicate, and differentiate into new myocytes and vascular structures, which connect to the unaffected ventricle. This process resulted in a 68% decrease in mortality, a 40% reduction in infarct size, and a 70% decrease in diastolic stress. The new myocytes and vessels improved ventricular function and reduced cavitary dilation. The study also demonstrated that BMC can transdifferentiate into cardiac cells, including endothelial cells and smooth muscle cells, and that this process is influenced by tissue damage and the presence of pluripotent cells. The findings suggest that cytokine-mediated mobilization of BMC could be a noninvasive therapeutic strategy for myocardial regeneration in ischemic heart disease and other cardiac conditions. The study highlights the potential of BMC as a source of cardiac repair and the importance of understanding the molecular mechanisms underlying their transdifferentiation. The results indicate that BMC can replace dead cardiac tissue and restore heart function, offering a promising approach for treating heart disease.