Myocardial cell metabolism

Myocardial cell metabolism comprises the network of metabolic pathways and regulatory nodes in cardiac myocytes responsible for generating and using energy substrates, including fatty acids, glucose, ketones, and amino acids[2][7][6]. Dysregulation of these pathways contributes to cardiac diseases such as heart failure and ischemic injury, and multiple enzymes, transporters (e.g., CD36), and signaling molecules within these pathways are recognized as therapeutic targets[1][2][3]. Pharmacological strategies aim to optimize substrate utilization, protect mitochondrial function, reduce oxidative stress, and enhance energy efficiency during pathological states[2][6]. However, "myocardial cell metabolism" as a phrase describes an ensemble of processes rather than a discrete molecular target and should not be used as a canonical drug target or receptor entry[1][2].

Other names

cardiac metabolismmyocardial metabolism

Inhibition of fatty acid oxidation (increases glucose utilization) Activation of pyruvate dehydrogenase (promotes glucose oxidation) Stimulation of ketone metabolism (increases energy efficiency) O-GlcNAcylation modulation (improves cell survival under stress) Inhibition of mitochondrial succinate metabolism (reduces reperfusion injury) Mitochondrial ROS scavenging (reduces oxidative damage)