Table 6.

Main studies on DNA methylation in obstructive sleep apnea syndrome (OSAS)/intermittent hypoxia (IH)

Gene name	Methylation level	Original source	Main findings	Reference
FOXP3	Hyper	Blood of OSAS children with and without high hsCRP	In OSAS children with increased systemic inflammatory response, methylation of the FOXP3 gene is more likely to increase, which may provide potential biomarkers for terminal organ susceptibility	Kim et al. (2023)485
AOEs	Hyper	Carotid body and adrenal medulla of rats exposed to IH	The persistent cardiopulmonary abnormality caused by IH is due to the long-term inhibition of the AOE gene by DNA methylation, resulting in a continuous increase in ROS levels in the carotid body chemosensory reflex pathway	Nanduri et al. (2017)487
IL1R2	Hypo	Blood of sleep-disordered breathing (SDB) patients with ODI >30 and SDB patients with ODI ≤30	IL1R2 hypomethylation and AR hypermethylation might be important determinants of disease severity	Chen et al. (2016)488
AR	Hyper
NPR2	Hypo	Blood of SDB patients with excessive daytime sleepiness (EDS) and SDB patients without EDS	NPR2 hypomethylation and SP140 hypermethylation might be biomarkers of EDS in patients with OSAS.
SP140	Hyper
eNOS	Hyper	Blood of OSAS children	Endothelial dysfunction caused by eNOS hypermethylation	Kheirandish-Gozal et al. (2016)706
Ace1 Agt	Hypo	CD31+ endothelial cells isolated from the mesenteric arteries of IH-exposed mice	IH-exposed mice had higher DNA methylation levels of Ace1 and Agt genes, which led to persistent changes in the renin-angiotensin system regulation and endothelial function, eventually leading to hypertension	Chu et al. (2015)707
FPR1	Hypo	Blood leukocyte of OSAS patients	Aberrant DNA methylation of the FPR1/2/3 gene in OSAS patients may be involved in the severity of the disease and the occurrence of diabetes mellitus or cardiovascular disease.	Chen et al. (2020)708
FPR2	Hyper
FPR3