Mice with CM lacking GATA4, a transcription factor that directly binds the VEGF-A promoter, show a poor capillary density in their hearts, while overexpression of GATA4 markedly improves cardiac vascularization and function following myocardial infarction by promoting angiogenesis (via VEGF-A production), hypertrophy, and inhibiting apoptosis [86,87]. Here, GATA4 is linked to myocardial infarction.