Review examining the emerging evidence for MOTS-c deficiency in obstructive sleep apnea, proposing that intermittent hypoxia-driven mitochondrial dysfunction suppresses MOTS-c production and that MOTS-c may serve as both a biomarker of OSA severity and a therapeutic target for the metabolic and cardiovascular complications that accompany chronic intermittent hypoxia. Positions MOTS-c restoration as a potential intervention in OSA. Provides a focused mechanistic argument for MOTS-c as a therapeutic target in OSA—where current treatment (CPAP) improves symptoms but does not directly correct the mitochondrial dysfunction underlying metabolic sequelae, suggesting MOTS-c supplementation as a complementary approach.
Edwards, Bradley A; Joosten, Simon A; Landry, Shane A