Cortese, ReneGileles-Hillel, AlexKhalyfa, AbdelnabyAlmendros López, IsaacAkbarpour, MahzadKhalyfa, Ahamed A.Qiao, ZhuanhongGarcia, TzintzuniAndrade, JorgeGozal, David2018-09-032018-09-032017-02-272045-2322https://hdl.handle.net/2445/124205Obstructive sleep apnea (OSA) affects 8-10% of the population, is characterized by chronic intermittent hypoxia (CIH), and causally associates with cardiovascular morbidities. In CIH-exposed mice, closely mimicking the chronicity of human OSA, increased accumulation and proliferation of pro-inflammatory metabolic M1-like macrophages highly expressing CD36, emerged in aorta. Transcriptomic and MeDIP-seq approaches identified activation of pro-atherogenic pathways involving a complex interplay of histone modifications in functionally-relevant biological pathways, such as inflammation and oxidative stress in aorta macrophages. Discontinuation of CIH did not elicit significant improvements in aorta wall macrophage phenotype. However, CIH-induced aorta changes were absent in CD36 knockout mice, Our results provide mechanistic insights showing that CIH exposures during sleep in absence of concurrent pro-atherogenic settings (i.e., genetic propensity or dietary manipulation) lead to the recruitment of CD36(+)high macrophages to the aortic wall and trigger atherogenesis. Furthermore, long-term CIH-induced changes may not be reversible with usual OSA treatment.application/pdfengcc-by (c) Cortese, Rene et al., 2017http://creativecommons.org/licenses/by/3.0/esSíndromes d'apnea del sonOxigen en l'organismeObesitatInflamacióMorbiditatMalalties cardiovascularsSleep apnea syndromesOxygen in the bodyObesityInflammationMorbidityCardiovascular diseasesinfo:eu-repo/semantics/article6783212018-09-03info:eu-repo/semantics/openAccess28240319