CHAT and heart failure: Heart-specific ChAT knockdown (hChAT KD) mice, developed by simultaneously overexpressing three ChAT mRNA-specific microRNAs in the heart, showed typical cardiac dysfunction with enhanced expression of heart failure markers, dysregulated expression of glucose metabolism-related molecules, increased ROS exposure in the heart, impaired cardiac NO production, poor angiogenesis, blunted vagus nerve activity, and disturbed association between NO synthase 1 and SERCA2 protein.