GCN5‐Mediated Lactylation of YY1 Promotes Diabetic Cardiomyopathy by Activating Twist1‐Dependent EndMT
GCN5 was upregulated in diabetic hearts and endothelial cells, and its knockdown reduced Twist1‐dependent EndMT in HG‐treated HUVECs, and this GCN5‐YY1‐Twist1 axis may offer novel therapeutic targets for DCM management.