Caspases in myocardial infarction.

The discovery of apoptosis sheds a new light on the role of cell death in myocardial infarction and other cardiovascular diseases. There is mounting evidence that apoptosis plays an important role at multiple points in the evolution of myocardial infarction, and comprises not only cardiomyocytes but also inflammatory cells, as well as cells of granulation tissue and fibrous tissue. It appears that apoptosis contributes to cardiomyocyte loss in the border zone and in remote myocardium in the early phase, as well as months after myocardial infarction, thus playing a role in remodeling and development of heart failure after myocardial infarction. Apoptosis, being a highly regulated process, is a potential target for therapeutic intervention. Caspases are the key effector molecules in apoptosis, and are therefore a particularly attractive target for pharmacological modulation of apoptosis. Although several potential therapeutic agents have been tested in animal models of ischemia/reperfusion heart injury with some success, nearly none of the specific antiapoptotic agents have reached the stage of clinical research.