In an in vivo study, we constructed an acute MI model, and under treatment with differently handled MSCs (Vector-MSCs or IL33-MSCs), echocardiography and Masson trichrome staining experiments indicated that overexpression of IL-33 in MSCs could enhance the left ventricular ejection fraction and fractional shortening and reduce heart tissue fibrosis (Fig. 7a–d). Here, IL33 is linked to myocardial infarction.