Grant: Project Grant

Heart attacks are a major cause of death around the world. When blood flow to a region of the heart is blocked (called ischemia) and then restored by doctors (called reperfusion), the heart can get damaged. This damage has been largely shown to result from harmful molecules called ROS (Reactive Oxygen Species) that are made in tiny parts of cells called mitochondria. Our research has shown that a protein called ROMO1, found in mitochondria, helps make ROS. While not much is known about ROMO1 in heart cells, our preliminary findings suggest that ROMO1 may be very important in ischemia/reperfusion injury. We found that when ROMO1 is "turned off" in heart cells, the heart makes less ROS during ischemia/reperfusion injury, which protects it from damage. We also discovered that hearts from male and female mice respond differently when ROMO1 is removed, with hearts from females not getting as much protection. This means ROMO1 might affect hearts differently depending on sex. Based on this, our hypothesis is that ROMO1 in heart cells is mainly responsible for making ROS and that this increases during ischemia/reperfusion. We also hypothesize that if we remove ROMO1, we might reduce the damage. However, these findings are only preliminary and much more research is needed to confirm this. Nevertheless, if we are able to confirm this, our research could uncover how this protein works in both healthy and damaged hearts and if ROMO1 turns out to be harmful during heart attacks, we could try to block it with medicine to protect the heart.