SLC38A2 and heart failure: Concurrently, amino acid transporters like SLC25A1 and SLC38A2 drive metabolic adaptations—SLC25A1 mutations disrupt citrate export, forcing reliance on glutaminolysis for nucleotide synthesis in hypertrophic cardiomyocytes, whereas SLC38A2 upregulation in heart failure fuels anaplerotic reactions at the cost of ammonia toxicity [100].