Research/Areas of Interest:

In response to physiological stress, the heart undergoes structural and functional changes known as pathologic cardiac remodeling. The Blanton lab has identified a direct role of the cGMP-dependent protein kinase 1α (PKG1α) in opposing pathologic cardiac remodeling, therefore PKG1α kinase substrates represent potential therapeutic targets in heart failure.

My project focuses on the role of mixed lineage kinase 3 (MLK3) which has been identified as a direct substrate and effector of PKG1α. Whole-body genetic deletion of MLK3 in mice leads to increased cardiac dysfunction and remodeling after pressure overload, and prevents the therapeutic effect of cGMP augmentation on LV function. However, whole-body MLK3 deletion also causes hypertension, and thus may confound the above findings. MLK3 is widely expressed in multiple tissues throughout the body and has been shown to mediate the impact of PKG1α on cardiac function, but controls blood pressure and vascular stiffness through separate mechanisms. My project will test the hypothesis that MLK3 opposes left ventricle dysfunction through a blood pressure-independent function specifically in the cardiac myocyte.

Education

BS, Biomedical Engineering, Worcester Polytechnic Institute, Worcester, MA