Abstract

The S100 family of EF-hand Ca2+-binding proteins S100A1, S100B and S100A6 are implicated in the pathophysiology of myocardial ischemia-reperfusion (I/R). S100A6 over-expression results in decreased cardiomyocyte apoptosis in vitro. Previously, we showed that after I/R, S100A6 gene expression progressively increases within infarct and peri-infarct regions of the left ventricular (LV) myocardium, well after early apoptosis, LV dilatation and systolic dysfunction. We hypothesized that S100A6 overexpression by ultrasound-targeted microbubble destruction (UTMD) would ameliorate I/R injury.

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