Review highlights DJ-1's role in glucose regulation across pancreatic, hepatic, and adipose tissues, suggesting redox balance is crucial for metabolic health.
DJ-1 (PARK7), originally characterized in Parkinson's disease, is increasingly recognized as a redox-sensitive regulator of systemic metabolism. Acting through oxidation-dependent modulation of Cys106, DJ-1 integrates cellular redox cues with mitochondrial function, insulin signaling, and stress adaptation pathways. In pancreatic β-cells, it preserves stimulus secretion coupling by stabilizing mitochondrial ATP production. In liver and adipose tissue, DJ-1 maintains insulin responsive signaling and metabolic flexibility through PTEN-PI3K-Akt and antioxidant networks. Loss or over-oxidation of DJ-1 disrupts interorgan glucose coordination, linking chronic redox imbalance to dysglycemia. This review positions DJ-1 as a metabolic sentinel translating oxidative inputs into integrated glucose regulatory outputs.
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Jayasingha et al. (2026) studied this question.
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