Methionine sulfoxide reductase A (MSRA)

Methionine sulfoxide reductase A (MSRA) is an enzyme that catalyzes the stereospecific reduction of methionine-S-sulfoxide (Met-SO) residues in proteins and free amino acids back to methionine, thereby repairing oxidative damage to proteins caused by reactive oxygen species[1][2][3][4]. MSRA activity contributes to antioxidant defense, helps maintain protein function, and may regulate cellular functions by reversible oxidation of methionine residues. MSRA is highly expressed in tissues susceptible to oxidative stress, such as the brain, liver, and kidney, and its loss or dysfunction is associated with increased oxidative protein damage, accelerated aging, impaired neurological function, and increased sensitivity to oxidative stress. There is also emerging evidence for MSRA's role in modulating protein ubiquitin-like modifications, particularly in archaea, suggesting broader roles in protein quality control under oxidative stress[4]. Overexpression in animal models has been linked to lifespan extension, while deficiency is linked to shortened lifespan and increased stress sensitivity[2][3]. There are no clinically approved drugs specifically targeting MSRA as of the most recent research.

Other names

Mitochondrial peptide methionine sulfoxide reductasePeptide Met(O) reductasePMSRPeptide-methionine (S)-S-oxide reductaseProtein-methionine-S-oxide reductaseCytosolic methionine-S-sulfoxide reductasePeptide methionine (O) reductase

Catalyzes thioredoxin-dependent reduction of methionine-S-sulfoxide residues in proteins and free methionine back to methionine[2][1]. Maintains protein function by repairing oxidative damage.