SMAD1 and myocardial infarction: Conversely, inhibition of miR-26a enhanced expression of Smad1 and promotes robust angiogenesis, which is associated with decreased myocardial infarct size and improved heart function, suggesting that miR-26a acts as a critical regulator of angiogenesis in ECs in a Smad1 dependent manner (Icli et al., 2013[41]).