In addition, abundant amounts of cytosolic class II HDAC4 and HDAC5 were demonstrated in adult mouse heart (Figure 9), TSA-treated heart demonstrated a diminished level of HDAC4 and HDAC5 (data not shown), supporting that class II HDACs serves as a potentially important target in modulation of acute myocardial ischemia and reperfusion injury through HDAC inhibition. This evidence concerns the gene HDAC5 and myocardial ischemia.