A study in mice and human keratinocytes demonstrated that the miR-483-3p 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 mouse model of acute myocardial infarction, the miR-483-3p was downregulated in the infarct region, and its overexpression reduced cardiomyocyte apoptosis and infarct size while improving cardiac function by targeting Cdk9 [Xue et al. DOI:10.1161/JAHA.122.026160].