In the healthy heart, it appears that expression of miR-133a and miR-30 are able to control ECM turnover by maintaining low secreted levels of the profibrotic cytokines TGF-β and connective tissue growth factor (CTGF/CCN2); a number of reports have demonstrated that miR-133a and miR-30 are downregulated in rodent and human heart failure [59,60]. This evidence concerns the gene CCN2 and heart failure.