RHOC and myocardial infarction: In conclusion, the current study provided evidence that M2Ms may mediate cardiac fibrosis after MI by releasing SEVs containing circUbe3a and that circUbe3a regulates RhoC expression, which is reversed by miR-138-5p, ultimately indicating that circUbe3a plays a role in promoting the proliferation, migration, and myofibroblastic transformation of CFs through the circUbe3a/miR-138-5p/RhoC axis.