Moreover, overexpression of CTRP3 improved left ventricular function, attenuated myocardial infarct size and apoptosis, and suppressed ROS, MDA and cTn-I levels in mice subjected to I/R injury compared with mice in the sham group, indicating that CTRP3 has a protective effect on mice subjected to myocardial I/R injury. The gene discussed is TNNI3; the disease is myocardial infarction.