A common pathomechanism in PPCM involves the angiostatic 16kDa-prolactin (16kDa-PRL) fragment, which via NF-κB-mediated upregulation of microRNA-(miR)-146a induces vascular damage and heart failure.
The effects of miR-146a inhibition on HF pathophysiology were examined by transducing a tough decoy of miR-146a into mice subjected to transverse aortic constriction. miR-146a inhibition improved cardiac contractile function and normalized SUMO1 expression.
Interestingly, a 1,000-fold increased expression of miR-146a was observed in CACs of CHF patients compared to CTR, along with decreased expression of IRAK1 protein.