In adult male mice, myocardial infarction significantly inhibits adipocyte CTRP3 expression and reduces plasma CTRP3 levels, and CTRP3 replenishment improves the survival rate, restores cardiac function, attenuates cardiomyocyte apoptosis, increases revascularisation, and dramatically reduces interstitial fibrosis, and the protective effect of adipocyte-conditioned medium against hypoxia-induced cardiomyocyte injury is significantly blunted when CTRP3 is knocked down [28]. The gene discussed is C1QTNF3; the disease is myocardial infarction.