AGT and myocardial infarction: In addition, we also notice that HDAC5 is reported to be a repressor of angiogenesis in endothelial cells41 and NaBu is found to promote angiogenesis in the heart of HFD‐induced diabetic and myocardial infarction animals.31, 38 Angiogenesis is a cardiac remodelling response, and capillary density is observed to be reduced in pathological hypertrophy.42 These results indicate that HDAC5 may contribute to Ang II‐induced cardiac hypertrophy by repressing angiogenesis, which could help explain how HDAC5 functions in endothelial cells but not in cardiomyocytes.