Grant: Operating Grant

Heart damage begins to occur after it has been deprived of oxygen (ischemia) for an extended period of time. While the immediate return of blood flow (reperfusion) to the heart is important, it too can damage the heart. Ischemia-reperfusion injury can significantly affect key components of the cell, such as mitochondria. In the heart, mitochondria provide about 90% of the energy for cardiac function. These dynamic organelles undergo continuous elongation and fragmentation processes to maintain proper function and meet cellular demands. Significant disruption in these processes caused by ischemia-reperfusion injury can impact the energy production of the cell resulting in dysfunction and death. Arachidonic acid (AA) is a molecule found in cell membranes that can be released in response to several stimuli such as hormones and cellular stress. Proteins within a cell break it down into active molecules called epoxyeicosatrienoic acids (EETs). These EETs are involved in regulating different functions in the body. Our reseach has demonstrated that EETs can limit mitochondrial injury. Thus, the objective of these studies is to advance our understanding of the EET-pathway targeting mitochondria and limiting injury. We propose targeting this pathway as a viable therapeutic strategy to prevent and/or treat mitochondrial damage caused ischemia-reperfusion injury. Results from this study will identify new regulatory mechanisms and advance our understanding of mitochondrial function.