Cardio Myogenesis Case

The purpose of this article is to discuss the role of myocytes and their contribution to the regeneration of the adult human heart. Myocytes are small cells that can differentiate and reenter the cell cycle, allowing for the cells of the heart to be regenerated over a course of every several years. Cell death in the heart is compensated by the regeneration of the cells through myocyte production. The formation of myocytes decreases with age. After a person experiences a myocardial infarction or any other trauma to the heart, the heart does not have the capability to regenerate its cells. Myocytes are only regenerated in the viable, non-traumatized portions of the heart. These conclusions were generally determined by the collection of iododeoxyuridine labeled myocytes from cancer patients. These results were correlated with the potential contribution of DNA repair, polyploidy, and cell fusion to the measurement of myocyte regeneration. According to the results, 22% of myocytes were generated each year with each cell having a life span of four and a half years and were diploidy. The conclusion of the experiment was that the human heart is capable of regenerating its own cells through its reserve of cardiac stem cells throughout its functioning life.

The purpose of this article was to discuss a therapeutic approach to help prevent systolic heart failure. Heart failure is a result of decreasing cardiac contractibility. Currently the most frequented therapies block neurohormonal activation with inhibitory pathways and neurotransmitters or increase contractility by indirectly activating pathways that increase myocyte calcium concentration. These eventually lead to higher mortality because it results in secondary complications. A new drug, omecamtiv mecarbila, would avoid these problems by directly activating the cardiac sarcomeres to improve cardiac performance. Omecamtiv mecarbila directly affects myosin by increasing the turnover rate of ATP, resulting in the increased number of myosin heads interacting with actin filaments. This leads to a greater force output of the muscle. Myosin has two different cardiac forms: alpha and beta. Studies show that individuals who have advanced heart failure have little to no alpha myosin present in their heart. Omecamtiv mecarbila would modify the beta myosin to increase the rate of force the heart muscle can exert.