MEF2A and myocardial infarction: Clinical trials using recombinant VEGFA to stimulate angiogenesis in patients with chronic myocardial ischaemia did not result in significant improvements in myocardial perfusion63, a result potentially explained by HDAC-mediated inhibition of MEF2 factors in these ischaemic regions: ischaemia has been shown to induce HDAC activity in the mouse heart after MI64, and pharmacological HDAC inhibition after MI can promote neovascularization and cardiac repair65.