Furthermore, Kore et al. [105] found that BMMSC-Exos treatment of MI significantly reduced interstitial and perivascular fibrosis in the ischemic heart and the expression of fibronectin in the infarct and peri-infarct regions; the underlying mechanisms involved suppression of the activation of p-38MAPK and NF-κB, which inhibited fibronectin, collagen 1, and collagen 3 expression. This evidence concerns the gene FN1 and myocardial infarction.