Abstract

Selenium is an essential trace element critical for cardiovascular health through its incorporation into antioxidant selenoproteins, such as glutathione peroxidase and thioredoxin reductase. The aim of this review is to explore the multifaceted role of selenium in maintaining cardiac structure and function, emphasizing its influence on redox homeostasis, ion channel regulation, and myocardial integrity. Selenium deficiency is linked to Keshan disease and other cardiomyopathies, with experimental models demonstrating impaired antioxidant defenses, mitochondrial dysfunction, and contractile failure. Supplementation restores antioxidant capacity, improves cardiac energetics, and reduces ischemia-reperfusion injury. Selenium also modulates calcium and potassium currents in cardiomyocytes, influencing action potential duration and arrhythmogenic risk. Electrocardiographic changes, including QT prolongation and low-voltage QRS complexes, are observed in selenium-deficient states and are reversible with selenium repletion. Studies using isolated perfused hearts and cardiac muscle preparations further elucidate selenium’s protective effects against oxidative stress and electrophysiological remodeling. Normal selenium concentrations in serum and myocardium are essential for optimal cardiac performance, while both deficiency and excess can be detrimental. Emerging therapeutic strategies, including selenium-based nanotechnology, highlight its potential in managing cardiovascular disease. Overall, selenium is a vital micronutrient in cardiac physiology, with implications for disease prevention and targeted intervention (200 words).