Using BMCs isolated from wild type (WT) mice and Sirt3 knockout (Sirt3KO) mice, the present study was: (i) to determine whether overexpression of apelin in WT-BMCs or Sirt3KO-BMCs improved cell therapy and enhanced cardiac repair; and (ii) to examine the potential molecular mechanism by which intramyocardial injection of apelin-BMCs improved cardiac repair in post-MI mice. The gene discussed is SIRT3; the disease is myocardial infarction.