A study in mice and human keratinocytes demonstrated that the mir-483 is upregulated during wound healing, peaking at the final closure stage, where its overexpression inhibits keratinocyte migration and proliferation by directly targeting MK2, MKI67, and YAP1, while its antagonism sustains proliferation [Bertero et al. DOI:10.1096/fj.10-168401]. In a separate study using mouse models of acute myocardial infarction, the mir-483 was downregulated in the infarct region, and its overexpression under therapeutic hypothermia inhibited hypoxia-induced cardiomyocyte apoptosis, reduced infarct size, and improved cardiac function by directly targeting Cdk9 [Xue et al. DOI:10.1161/JAHA.122.026160].