Mechanistic links between obstructive sleep apnea, cellular senescence and aging: The role of cardiometabolic dysfunction

Obstructive sleep apnea (OSA) is a common condition characterized by repeated airway obstruction during sleep, triggering physiological changes that resemble key features of cellular senescence—oxidative stress, mitochondrial dysfunction, and systemic inflammation. While senescence plays roles in tissue repair, its accumulation also drives chronic inflammation and immune dysregulation. The connection between OSA, senescence, and aging remains complex and underexplored. Mechanisms like the senescence-associated secretory phenotype (SASP), impaired immune surveillance, and reduced regenerative capacity may contribute to OSA-related morbidity. This review examines how senescence influences immune and molecular pathways in OSA, with a focus on cardiometabolic dysfunction, SASP-driven tissue remodeling, and hypoxia-induced damage. We also highlight emerging therapies targeting senescence, proposing that it acts not only as a byproduct of aging but as an active driver of OSA pathology, shaped by hypoxia, sleep disruption, comorbidities, and immune profiles.