Project 452736

Heart attack is a major health issue in Canada and it causes the blockage of heart blood vessels leading to the death of muscle cells in the affected areas of the heart. Unfortunately, the majority of the patients who are able to survive a heart attack will develop heart failure (a condition that the heart can no longer pump blood as well as before), because the dead muscle cells cannot be replaced by new muscle cells in the heart. Heart failure significantly limits quality of life, increases the risk of premature deaths and healthcare cost. The objective of this project is to study the role of a protein, which is increased in the heart after heart attack, in mediating the death of heart muscle cells after an heart attack. This work may uncover novel mechanisms of muscle cell death and the development of heart failure. We will use laboratory animals (rats and mice) and ligate a major blood vessel in their hearts to mimic the blockage of heart blood vessels and heart attack in patients. We will then examine if the protein of interest is increased in these animal hearts after the artery ligation. Next, we will use transgenic mice in which this protein is genetically deleted, and use special techniques (e.g., ultrasound for imaging the heart) to examine if this protein inhibition can reduce or slow down the development of heart failure. This project is expected to elucidate novel mechanisms underlying muscle cell deaths after a heart attack and guide the designing of new therapies to reduce heart failure, improve quality of life, reduce premature deaths, and reduce healthcare cost.