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Both ischemia and ischemia/reperfusion trigger cell death via mechanisms that involve class I HDACs. Inhibition of HDAC activity reduces infarct size. Post-infarct stresses induce cardiomyocyte hypertrophy, cell death (e.g. apoptosis) and fibrosis. Again, HDAC inhibitors are capable of blocking elements of these detrimental biological processes and preserve cardiac function.
