Since the prognosis for heart failure patients is usually grim, any therapy that delays the transition between a compensated, hypertrophied heart to a decompensated, failing one would have a tremendous impact on the quality of life and life expectancy of heart failure patients. The goal of my research program is to understand the normal and abnormal functioning of the heart at a basic molecular level by characterizing changes in cardiac gene expression that accompany the pathogenesis of heart disease in the mouse. Differential display RT-PCR has identified novel mRNAs that exhibits altered expression in a transgenic mouse model of cardiomyopathy and early heart failure. Characterization of these novel genes will include analysis of their basic cellular and molecular properties as well as the genetic manipulation of these genes in mice. Selected References Vikstrom, K.L., S.M. Factor, and L.A. Leinwand.
Mice expressing mutant myosin are a model for hypertrophic cardiomyopathy.
Vikstrom, K.L., T. Bohlmeyer, S.M. Factor, and L.A. Leinwand. Hypertrophy, pathology, and molecular markers of cardiac pathogenesis.