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A few years ago, we asked a simple question “How do cardiomyocytes die during myocardial infarction”.

We found that immune cells were contributing to cardiomyocyte cell death and gamma-delta T cell-mediated cardiac cell death appears to be a major mechanism. We hypothesise is that targeting these cells should further reduce infarct size after MI/ischemia-perfusion injury and reduce the incidence of MI-induced heart failure. The studies are not yet completed, but preliminary results are sufficient to support our hypothesis. We will continue to study mechanistic understanding and to test potential therapeutic strategies.

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