Abstract
Ischemic heart disease continues to be one of the major causes of death in the developed world despite improvements in treatment. 30% of non-lethal myocardial infarctions will develop heart failure symptoms. Improved survival of the myocardium is a need in clinical practice. Our group has previously shown that Celastrol, along with a synthetic HSP90 inhibitor analog have the potential to reduce infarct size when given as a postconditioning agent at the moment of reperfusion. The objective is to evaluate the rapid cardioprotective mechanisms of a novel formulation of the HSP90 inhibitor compound on two cell lines: rat H9c2 cardiomyoblasts and Human induced pluripotent stem cell-derived cardiomyocytes (iPSC-CMs).
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