MSRB2 (methionine sulfoxide reductase B2) is a mitochondrial protein that catalyzes the reduction of methionine (R)-sulfoxide back to methionine, serving as a critical antioxidant enzyme. Its primary function involves scavenging reactive oxygen species and maintaining protein homeostasis under oxidative stress conditions 1. Mechanistically, MSRB2 operates through multiple pathways: it reduces oxidized methionine residues in proteins, promotes mitophagy by reducing Parkin methionine oxidation to facilitate selective removal of damaged mitochondria 2, and reduces oxidized actin monomers to stabilize cytokinetic bridges during cell division 3. Additionally, MSRB2 regulates APP processing and Tau phosphorylation through JNK and ERK signaling pathways 1. Clinically, MSRB2 shows relevance across multiple diseases. Reduced MSRB2 expression is associated with Alzheimer's disease pathology; overexpression decreases amyloid-beta production and tau phosphorylation 1. MSRB2 is downregulated in osteoarthritis, where its overexpression mitigates chondrocyte oxidative stress and apoptosis 4. Low MSRB2 expression in Parkinson's disease correlates with reduced mitophagy 2, while increased expression in diabetes protects against cardiac complications 5. MSRB2 also serves as a diagnostic biomarker for tuberculosis 6 and sepsis 7, identifying it as a therapeutic target across neurodegenerative, metabolic, and inflammatory diseases.