The results shows that silencing Wisper could alleviate myocardial infarction-induced fibrosis and cardiac dysfunction through upregulating myocardial fibroblasts Col3a1, Fn1, Tgfb2, and aSma expression.176 These results provide new insights into the pathogenesis of heart failure and contribute to enhance diagnostic performance and treatment strategies for heart failure, thereby improving the long-term prognosis of heart failure. Here, TGFB2 is linked to heart failure.