Figure 8. Schematic illustration of PI16 protecting from apoptosis and left ventricular remodeling by inhibiting the HDAC1‐Wnt‐β‐catenin axis.

The expression of HDAC1 in cardiomyocytes is upregulated after MI, which enhances canonical Wnt/β‐catenin pathway by increasing Wnt3a expression, leading to cardiomyocyte apoptosis and cardiac remodeling. PI16 inhibits the expression of HDAC1 and thus suppresses the activation of the downstream Wnt/β‐catenin pathway, thereby protecting against injury and remodeling after MI. HDAC1 indicates class I histone deacetylase; IWR‐1‐endo, the inhibitor of Wnt signaling; MI, myocardial infarction; PI16, peptidase inhibitor 16; and Wnt,wingless‐type MMTV integration site family.