Abstract
Despite improvements in treatment, Ischemic heart disease is still the second cause of death in Canada. Even in non lethal cases, up to 30% of myocardial infarctions will develop heart failure symptoms, thus the need for improved myocardial survival is a clinical unmet need. Our group has previously shown that Celastrol family HSP90 inhibitors have the potential to reduce infarct size when given at the moment of reperfusion. Nevertheless, its mechanisms of action are not fully understood. The objective is to evaluate the cytoprotective mechanisms, focusing in mitochondrial effects, underpinning the observed rapid cardioprotection by a Celastrol compound.
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