C1QTNF3 and myocardial infarction: The expression and production of CTRP3 are significantly reduced post-MI, [60] and replenishment of CTRP3 attenuates post-MI pathologic remodeling, including reducing heart size and cardiomyocyte apoptosis, increasing cardiomyocyte survival/regeneration, attenuating remote area interstitial fibrosis, as well as enhancing infarct border zone revascularization [60].