Its protective effects are partially mediated through direct suppression of the Adamts1 gene: on one hand, miR-181a knockout significantly exacerbates cardiac dysfunction and remodeling in mice post-myocardial infarction, with this effect directly correlated to increased Adamts1 expression; On the other hand, overexpression of miR-181a exerts cardioprotective effects by suppressing Adamts1 expression [30]. Here, ADAMTS1 is linked to myocardial infarction.