{"id":694947,"date":"2025-10-15T13:45:12","date_gmt":"2025-10-15T10:45:12","guid":{"rendered":"https:\/\/buradabiliyorum.com\/en\/study-highlights-how-sleep-apnea-accelerates-cellular-aging-and-cardiometabolic-decline\/"},"modified":"2025-10-15T13:45:12","modified_gmt":"2025-10-15T10:45:12","slug":"study-highlights-how-sleep-apnea-accelerates-cellular-aging-and-cardiometabolic-decline","status":"publish","type":"post","link":"https:\/\/buradabiliyorum.com\/en\/study-highlights-how-sleep-apnea-accelerates-cellular-aging-and-cardiometabolic-decline\/","title":{"rendered":"Study highlights how sleep apnea accelerates cellular aging and cardiometabolic decline"},"content":{"rendered":"
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A new review<\/a> published in Sleep Medicine Reviews<\/i> sheds light on the biological mechanisms that may explain why patients with obstructive sleep apnea (OSA) face higher risks for heart disease, diabetes and other age-related conditions.<\/p>\n

The study, led by researchers at Marshall University Joan C. Edwards School of Medicine, details how OSA-induced stressors can trigger cellular senescence\u2014effectively accelerating the aging process at the molecular level.<\/p>\n

OSA is typically recognized as a disorder of repeated airway collapse during sleep that causes oxygen deprivation and fragmented sleep. However, the authors argue that its effects extend far beyond nighttime breathing disturbances.<\/p>\n

The review synthesizes evidence showing that intermittent hypoxia, oxidative stress, mitochondrial injury and chronic inflammation caused by OSA activate pathways linked to cellular senescence. These senescent cells, in turn, release inflammatory molecules\u2014known as the senescence-associated secretory phenotype (SASP)\u2014that contribute to vascular remodeling, insulin resistance, immune dysregulation and other hallmarks of cardiometabolic disease.<\/p>\n

The authors, which include Sarfraz Ahmed, Ph.D.; David Gozal, M.D., M.B.A., Ph.D. (Hon); and Abdelnaby Khalyfa, M.S., Ph.D., all of Marshall University, propose that these senescence-driven processes may help explain the earlier onset and higher prevalence of hypertension, atherosclerosis, metabolic syndrome and other age-associated conditions in people with OSA.<\/p>\n

They suggest that treating sleep apnea with continuous positive airway pressure (CPAP) alone may not fully reverse the downstream cardiometabolic damage. Instead, combining conventional therapies with emerging interventions that target senescent cells\u2014such as senolytic or senomorphic drugs\u2014could offer new opportunities to blunt OSA-related cardiovascular and metabolic risk.<\/p>\n

While further research is needed to validate these mechanisms in clinical settings and to identify reliable, noninvasive biomarkers of senescence that could guide future treatments, the review underscores the importance of viewing OSA as more than a sleep-disordered breathing condition.<\/p>\n

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More information:<\/strong>
\n Sarfraz Ahmed et al, Mechanistic links between obstructive sleep apnea, cellular senescence and aging: The role of cardiometabolic dysfunction, Sleep Medicine Reviews<\/i> (2025). DOI: 10.1016\/j.smrv.2025.102170<\/a><\/p>\n<\/div>\n

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\n Citation<\/strong>:
\n Study highlights how sleep apnea accelerates cellular aging and cardiometabolic decline (2025, October 15)
\n retrieved 15 October 2025
\n from https:\/\/medicalxpress.com\/news<\/a>\/2025-10-highlights-apnea-cellular-aging-cardiometabolic.html\n <\/p>\n

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