Fig. 8.

Graphical mechanism summary: Human cTnIAAb interacts with ENO1 present in the myocardial membrane and induces apoptosis of cultured cardiomyocytes. Human cTnIAAb can trigger cardiomyocyte apoptosis via binding membrane ENO1, increasing ENO1 expression, promoting phosphorylation of PTEN Ser380, and suppressing Akt activity in the mouse model of cTnImAb-induced myocardial injury. This induces the pro-apoptotic Bax and suppresses the anti-apoptotic Bcl2 expression resulting in cardiomyocyte apoptosis.