Heart failure is a leading cause of hospitalization and mortality in the US. Dr. Matsui and his colleagues focus on understanding the mechanism and signal transduction pathway underlying cardiac dysfunction that arises from myocardial infarction and cardiac hypertrophy, apparent risk factors for heart failure. Specifically, Dr. Matsui's interests center around the role of the mammalian target of rapamycin (mTOR), which is intimately related to the insulin/phosphatidylinositol 3-kinase (PI3K)/Akt signal transduction pathway. This signal transduction pathway is known to be important in cell survival, cardiac hypertrophy and cardiac remodeling. In order to investigate the role of mTOR in the heart, Dr. Matsui and his colleagues utilize a variety of in vitro, in vivo, and ex vivo models. Recombinant DNA is employed in both cells via the use of gene transfer and animals via the generation of transgenic mice. In fact, Dr. Matsui and his colleagues are studying mice engineered with cardiac-specific overexpression of mTOR in order to see if changes in disease processes related to heart failure occur. Several stresses including ischemia-reperfusion and pressure-overload are employed in order to mimic disease states found in heart failure. Hopefully, an enhanced comprehension of the mechanism underlying cardiac dysfunction will lead to the identification of novel therapeutic targets along the mTOR signal transduction pathway for the treatment of heart failure.