Obstructive sleep apnea is a growing worldwide health problem. The landmark feature of OSA is a chronic intermittent hypoxia (CIH) responsible for multiple organ damages including heart diseases. Under several pathophysiological conditions such as aging, vWAT senescence drives myocardial alterations through the release of profibrotic factors. Our lab has demonstrated that CIH profoundly alters both vWAT and heart structure and function, but little is known regarding their interactions in the context of CIH. Thus, our primary objective is to demonstrate that CIH induces a premature vWAT senescent phenotype, responsible for subsequent heart dysfunction. From this, we aim at i) bringing the proof-of-concept that strategies targeting CIH-induced vWAT senescence exert beneficial effects on cardiac alterations, and ii) identifying CIH-specific circulating biomarkers that may ultimately contribute to cardiac dysfunction.