Extracellular vesicles derived from trophoblastic stem cells (TSCs) could transfer miRlet-7i to myocardial cells, inhibit the inflammatory response, and reduce myocardial cell apoptosis and fibrosis by downregulating YAP1 activity, accompanied by a decrease in the expression levels of the YAP target genes ctgf and TEAD. Thus, DOX-induced myocardial remodeling and heart failure can ultimately be reversed, thereby improving dilated cardiomyopathy and cardiac dysfunction caused by doxorubicin treatment (Ni et al., 2020). Here, CCN2 is linked to heart failure.