UCLA

Acute myocardial ischemic-reperfusion (IR) injury remains a widespread, unresolved clinical problem. While current therapies in animal IR injury models target delaying of the mitochondria permeability transition pore, none have shown success in human trials. Therefore, novel therapies are critical to limit IR injury and improve patient outcomes following reperfusion intervention. Our lab showed that intralipid (ILP), a safe fat emulsion, protects the heart against IR injury in rodent models. The exact molecular mechanisms by which ILP confers this cardioprotection is unclear and deciphering it could help develop more targeted effective reperfusion intervention for myocardial infarct. microRNAs are promising mediators in ILP cardioprotection as they regulate gene expression in IR injury molecular pathways. Here, we show that ILP normalizes miR-1 expression in hearts subjected to IR injury using a longer reperfusion time; this is associated with reduced infarct size and reduced apoptosis in cardiomyocytes subjected to hypoxia-reoxygenation. My findings will uncover mechanisms of ILP-mediated cardioprotection, which should lead to a novel therapeutic strategy against acute myocardial IR injury.