We have generated three humanized cardiac-specific transgenic mouse models of cardiomyopathy using standard Cre-loxP recombination methods. We are characterizing the physiological, functional and molecular aspects of these mice models specifically we are studying the following pathological hypertrophic parameters

1. Enlargement of cardiomyocytes
2. Reactivation of fetal genes
3. Fibrosis of extracellular matrix
4. Sarcomeric reorganization
5. Activation of MAPkinase pathways
6. Decreased cardiac function

We are also using these pre-clinical models for translational research.