Table 1: Normal functions of representative selenoproteins relevant to the cardiovascular system and their corresponding clinical deficient features.

Selenoprotein Normal Functions Clinical Features of Deficiency [ref]
Thioredoxin reductase ▪ Disulfide reduction
▪ Maintenance of cellular redox homeostasis
Dilated Cardiomyopathy in humans [5]
Glutathione peroxidase 1 ▪ H2O2 signaling
▪ Inactivation of hydroperoxides
▪ Maintenance of cellular redox homeostasis
Larger myocardial infarct size in a mouse model [76]
Methionine sulfoxide reductase A ▪ Prevention of the buildup of oxidized methionine residues in proteins Impaired myocardial contractility when stressed in a mouse model [77]
deiodinases ▪ Activation of T4 to T3
▪ Degradation of T3
▪ Regulation of catabolic homeostasis
Restrictive cardiomyopathy in a mouse model [78]
Selenophosphate Synthetase 2 ▪ Synthesis of selenophosphate required for the synthesis of selenoproteins No data on clinical features of deficiency [3]
Selenoprotein I ▪ Synthesis of phosphatidylcholine and phosphatidylethanolamine No data on clinical features of deficiency [3]
Selenoprotein M ▪ Maintenance of the redox homeostasis in the ER
▪ Facilitation of protein folding in the ER
No data on clinical features of deficiency [3]
Selenoproteins K and S ▪ Facilitating proteasome-mediated degradation of misfolded proteins in the ER No data on clinical features of deficiency [3]