Elizabeth Luczak

Cardiac hypertrophy is an enlargement of the heart due to signaling events in the cardiac myocyte in response to increased load on the heart.  Cardiac myocyte growth occurs in response to both exercise and disease, and this response is modified by gender.  One signaling molecule that has been linked to cardiac hypertophy is calcium/calmodulin-dependent kinase (CaMK).  CaMK has been shown to regulate both gene expression and intracellular Ca²⁺ handling in the heart, both of which play a role in cardiace hypertrophy.  CaMK is activated in disease models of cardiac hyperthophy, and recent data indicate that it is also activated in exercise models.  Furthermore, transgenic mice overexpressing CaMK in their hearts experience significant cardiac enlargment.  How CaMK is involved in regulating cardiac hypertrophy is still unclear.  My work is focused on determing the role of CaMK in regulating cardiac hypertrophy in both exercise and disease models.  I am using CaMKll overexpression transgenic mouse models to determine 1) the effects of overexpression of CaMKll on exercise capacity and cardiac adaptation to exercise, 2) the effects of CaMKll overexpression on pathologic models of hypertrophy, and 3) the role of gender in modifying the hearts response to CaMKll overexprssion.  These studeies will provide novel insight into how CaMK signaling contributes to cardiac hypertrophy.