Deletion of EMRE to protect hearts during Ischemia Reperfusion Injuries
The mitochondrial calcium uniporter (mtCU) is how calcium is taken up into the mitochondria. This calcium uptake is used as a precursor to the TCA cycle and therefore ATP energy production. If too much calcium is taken up leading to overload in the mitochondria, this can lead to the opening of the permeability transition pore which is the primary cause of cell death during ischemia reperfusion (I/R) events such as heart attacks. To protect cardiac cells during these types of ischemic stress events, there needs to be a decrease in the amount of calcium taken up. Essential mitochondrial regulator (EMRE) is a key component in the mitochondrial uniporter for calcium uptake, so deletion of EMRE could possibly help to prevent injury following an I/R event through reducing the amount of calcium uptake. Here we show how deletion of EMRE in mice leads to a decreased percentage of infarct, or damage in cardiac tissue following simulated I/R. These results indicate that EMRE has an influential effect on cardiac health following I/R injuries. Also, it further supports the idea that decreasing the amount of calcium taken up during I/R can contribute to greater mitochondrial health. These findings further the possibility of EMRE being a target for novel therapies aimed at decreasing the damage caused by heart attacks in patients prone to them. Overall, this could help to decrease the long term cardiac damage that often follows these I/R events.