The Laryngoscope · 2025
Lipofuscin: The Missing Link in the Worsening of Obstructive Sleep Apnea.
СтатьяПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод в очереди
Обработка статьи · этапы, ошибки и управление
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Fahl Kristine, Palomino Carlos Modesto Vera, da Silva Baptista Mauricio, Ciena Adriano Polican, da Silva Dantas Danielle Andrade, Sennes Luiz Ubirajara, Chacur Marucia, Cahali Michel Burihan
Аннотация
OBJECTIVES: There is a lack of evidence linking oxidative stress to muscle dysfunction and the worsening of obstructive sleep apnea (OSA). Lipofuscin is a permanent intracellular deposit that accumulates with aging or oxidative stress. Its increase in skeletal muscles may lead to limitations in muscle function, such as weakness and fatigue. We aim to investigate whether lipofuscin deposits in the upper airway muscles of patients with severe OSA are increased compared to those in patients with primary snoring or very mild OSA.
METHODS: We studied pharyngeal framework muscle tissue samples from non-obese adults, with one group having severe OSA and another having primary snoring or very mild OSA (snorer group). Lipofuscin was identified by analyzing staining patterns from Sudan Black B and fluorescence microscopy. We compared lipofuscin levels and distribution in the muscle fibers between the groups.
RESULTS: Despite presenting similar age and body mass index, patients with severe OSA exhibited markedly larger and more concentrated deposits of lipofuscin in the upper airway muscles, particularly along the borders of the muscle fascicles, compared to the snorer group.
CONCLUSION: Compared to primary snorers, patients with severe OSA accumulate lipofuscin in their pharyngeal muscles. Our findings may provide novel insight into the role of lipofuscin as both a marker and a cause of the aggravation of OSA, in light of a possible lipofuscin-induced progressive myopathy.
METHODS: We studied pharyngeal framework muscle tissue samples from non-obese adults, with one group having severe OSA and another having primary snoring or very mild OSA (snorer group). Lipofuscin was identified by analyzing staining patterns from Sudan Black B and fluorescence microscopy. We compared lipofuscin levels and distribution in the muscle fibers between the groups.
RESULTS: Despite presenting similar age and body mass index, patients with severe OSA exhibited markedly larger and more concentrated deposits of lipofuscin in the upper airway muscles, particularly along the borders of the muscle fascicles, compared to the snorer group.
CONCLUSION: Compared to primary snorers, patients with severe OSA accumulate lipofuscin in their pharyngeal muscles. Our findings may provide novel insight into the role of lipofuscin as both a marker and a cause of the aggravation of OSA, in light of a possible lipofuscin-induced progressive myopathy.