ADAMTS4 and myocardial infarction: Moreover, we manipulated the expression of Adamts4 with siRNA-mediated loss of function and TGF-β inhibitor studies in H9c2 cells to evaluate its regulation and dependency on TGF-β signaling since TGF-β has been long known to be a characteristic marker for inflammatory and fibrotic responses following pathological stress including MI, ischemia and reperfusion (I/R) injury16–20.