SLC38A1 and coronary artery disorder: SLC38A1 is an amino acid transporter, and alterations in its expression may affect the intracellular balance of amino acids, further influencing the synthesis of ferritin and other iron metabolism-related proteins (50).The functional network of these hub genes reveals that dysregulation of iron metabolism may participate in the pathological processes of CAD through multiple pathways, including oxidative stress, energy metabolism dysregulation, protein homeostasis imbalance, and autophagy abnormalities.