Disrupted erythrocyte S1P-eNOS axis promotes hypoxia, hypertension and fibrosis in obstructive sleep apnoea-hypopnoea syndrome

This study investigates the role of red blood cells (RBCs) in the pathogenesis of obstructive sleep apnoea-hypopnoea syndrome (OSAHS), specifically examining how disruptions in the sphingosine-1-phosphate (S1P) and endothelial nitric oxide synthase (eNOS) axis contribute to hypoxia, hypertension, and fibrosis. The authors aim to identify early biomarkers and potential therapeutic targets to mitigate the cardiovascular and renal consequences associated with OSAHS. Findings suggest that RBC dysfunction and altered metabolic pathways are critical in the disease's progression, with specific metabolites serving as sensitive indicators for diagnosis and treatment efficacy.