Recently, we created calreticulin deficient mouse and showed that calreticulin gene knockout is embryonic lethal. The same transduction pathway plays a role in cardiac hypertrophy and calreticulin protein is up regulated in the hypertrophied heart. Focus of our research supported by the Astra Pharma is on the role of calreticulin in cardiac hypertrophy. We investigate mechanisms responsible for activation of the calreticulin gene in cardiac hypertrophy. One important aspect of our work is to create a transgenic mouse model for studying cardiac hypertrophy using the calreticulin gene and other genes as markers of hypertrophy.
Heart diseases remain a major cause of early death in the Western population, including Canada.
Our studies will provide major insights into molecular mechanisms underlying control of cardiac genes expression in normal and diseased heart. This information will be invaluable for designing of new and more specific drugs. Our work is directly relevant to such fundamental clinical problems as hypertension, pressure overload, cardiac arrhythmias, myocardial infarction, and congenital heart disease.