DHRS7C is an NADH-dependent oxidoreductase that catalyzes the conversion of all-trans-retinol to all-trans-retinal, with primary roles in cardiac and skeletal muscle metabolism 1. The enzyme is localized to the sarcoplasmic reticulum membrane and regulates intracellular calcium homeostasis by repressing calcium release through the ryanodine receptor, potentially via local NAD/NADH and retinol/retinal alterations 1. DHRS7C promotes glucose uptake and muscle performance by activating PI3K and mTORC2-mediated AKT1 phosphorylation pathways, likely through all-trans-retinoic acid production. Expression is highly enriched in heart and skeletal muscle 2 and is downregulated by adrenergic stimulation and in heart failure 2, with expression inversely correlated with left ventricular dysfunction 3. In dilated cardiomyopathy, DHRS7C acts as a key regulator of glucose/energy metabolism 3, and computational studies identify it as a potential early-stage colorectal cancer biomarker 4. Right ventricular failure in pulmonary arterial hypertension shows DHRS7C downregulation, consistent with excessive autonomic activation 5. In hibernators, DHRS7C abundance increases during prehibernation, contributing to skeletal muscle preservation during prolonged inactivity 6.