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Disrupted erythrocyte S1P-eNOS axis promotes hypoxia, hypertension and fibrosis in obstructive sleep apnoea-hypopnoea syndrome
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DOI：10.1093/eurheartj/ehag405.png)
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Abstract
En 中文
Obstructive sleep apnoea-hypopnoea syndrome (OSAHS) has emerged as a global epidemic with profound cardiovascular and renal consequences, yet its early pathogenic mechanisms remain poorly understood. Whether red blood cells (RBCs) act as the primary hypoxia sensor that transduces intermittent apnoea into irreversible outcomes remains enigmatic. This study aims to define the pathogenic nature of RBCs during the progression of OSAHS with a goal of identifying early biomarkers and targeted treatments to prevent detrimental outcomes.
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