Thus, CTRP12 overexpression reduced cardiac apoptosis, oxidative stress, and inflammation and improved left ventricular function in rats subjected for 6 weeks to myocardial infarction produced by coronary artery ligation, whereas CTRP12 deletion enhanced remodelling and worsened left ventricular dysfunction [257]. The gene discussed is C1QTNF12; the disease is myocardial infarction.