%0 Journal Article %A B Santos %A L Gaspar %A C Carvalhas-Almeida %A A T Barros-Viegas %A S Carmo-Silva %A C Santos %A S Carvalho %A D Marques %A J Moita %A C Cavadas %A A R Álvaro %T Unraveling the impact of obstructive sleep apnea on senescent associate secretory phenotype %D 2021 %R 10.1183/23120541.sleepandbreathing-2021.82 %J ERJ Open Research %P 82 %V 7 %N suppl 7 %X Introduction: Obstructive Sleep Apnea (OSA), one of the most common sleep disorders worldwide has been suggested to promote aging by inducing cellular and molecular aging mechanisms (Gaspar, et al. 2017). Understanding OSA putative effect on aging might contribute to understand new strategies to improve OSA diagnosis and treatment but also to counteract aging.Aim: To investigate cellular senescence and senescent associate secretory phenotype (SASP), a hallmark of aging, in OSA patients and the impact of OSA treatment.Methods: A cohort of 9 adult male patients diagnosed with severe OSA was followed from the moment of diagnosis with polysomnography (PSG), up to 4 months and 24 months of treatment with continuous pressure positive mask (CPAP). SASP biomarkers were evaluated in OSA patients in comparison to age-matched controls and younger controls, both validated by PSG.Results: OSA patients show a deregulation of pro- and anti-inflammatory cytokine levels, in comparison with age-matched and young controls, an effect that is no longer observed after treatment. In addition, OSA patients show alterations in extracellular vesicles release that are not fully re-established upon CPAP treatment.Conclusion: These results suggest that OSA might induce SASP. CPAP treatment might partially re-stablish some alterations. Hence, OSA early diagnosis and specific treatment may constitute a new strategy to delay ageing.FootnotesCite this article as ERJ Open Research 2021; 7: Suppl. 7, 82.This is an ERS Lung Science Conference abstract. No full-text version is available. Further material to accompany this abstract may be available at www.ers-education.org (ERS member access only). %U