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Updated: May 6, 2026
Induction and Analysis of Oxidative Stress in Sleeping Beauty Transposon-Transfected Human Retinal Pigment Epithelial Cells
Published on: December 11, 2020
Biomarker-Based Analysis of the Association Between Obstructive Sleep Apnea Syndrome and Oxidative Stress: A
Yuyin Liu1, Suru Liu2, Jianhong Deng1
1Department of Otorhinolaryngology, Hospital of Chengdu University of Traditional Chinese Medicine, No.39 Shi-er-qiao Road, Chengdu, 610072, Sichuan Province, P.R. China.
Objective:
This study aimed to investigate the potential genetic association between obstructive sleep apnea syndrome (OSAS) and oxidative stress (OS) using multi- -dimensional Mendelian randomization (MR) analysis.
Methods:
We conducted bidirectional univariable MR analyses using FinnGen-derived OSAS genetic data and summary statistics for 16 oxidative stress biomarker indicators (OSBIs) from IEU OpenGWAS and GWAS Catalog, employing five methods with sensitivity analyses to evaluate robustness and heterogeneity. Multivariable MR (MVMR) was further applied to adjust for confounders and estimate the direct effect of OSAS on OSBIs.
Results:
OSAS might be a risk factor for elevated lactate (OR = 1.06, 95% CI = 1.02-1.11, p < 0.01). MVMR supported an independent causal effect (OR = 1.16, 95% CI = 1.02-1.32, p = 0.03), although significant heterogeneity suggests interpretation requires caution. Reverse MR suggested that decreased superoxide dismutase (OR = 0.96, 95% CI = 0.93-0.98, p < 0.01) and matrix metalloproteinase-9 (OR = 0.98, 95% CI = 0.96-0.99, p < 0.01) were associated with OSAS. Furthermore, MVMR suggested a potential effect of OSAS on elevated vitamin E levels (OR = 1.15, 95% CI = 1.01-1.32, p = 0.04).
Discussion:
Our study provides genetic evidence for a bidirectional causal relationship between OSAS and OSBIs. Potential mechanisms may include hypoxia-disordered glucose metabolism and a compensatory upregulation of the antioxidant system. Future research should utilize larger, multi-ethnic samples and incorporate a broader range of OSBIs to systematically delineate these relationships.
Conclusion:
OS is both a driver and a pathological consequence of OSAS.
