Related Experiment Video
Updated: May 20, 2026
Long-term Monitoring of Oxygen Consumption Rates in Highly Differentiated and Polarized Retinal Pigment Epithelial Cultures
Published on: August 16, 2024
Selective vulnerability of the macular ganglion cell layer to nocturnal hypoxia in obstructive sleep apnea: A 3-year
Zhiling Zhao1, Xiaoshuang Lyu1, Tianyue Xin2
1Department of Respiratory and Critical Care Medicine, Beijing Institute of Respiratory Medicine and Beijing Chao-Yang Hospital, Capital Medical University, Beijing Key Laboratory of Multimodal Intelligent Diagnosis and Treatment System for Respiratory Diseases, Beijing, China.
Objective:
To evaluate the association between nocturnal hypoxemia metrics in obstructive sleep apnea (OSA) and subclinical structural alterations of retinal neurons.
Methods:
In this prospective study, 79 newly diagnosed OSA patients underwent overnight polysomnography and spectral-domain optical coherence tomography. OSA-related nocturnal hypoxemia was assessed using the oxygen desaturation index (ODI). Associations between ODI and retinal parameters were assessed using linear mixed-effects models, and longitudinal structural changes were evaluated in 25 participants after 3 years.
Results:
Higher ODI was associated with reduced minimum ganglion cell layer (GCL) thickness (P = 0.011), whereas mean GCL showed a borderline association (P = 0.052). Peripapillary retinal nerve fiber layer (RNFL) thickness was not significantly associated with ODI (P = 0.466). GCL thinning demonstrated a focal distribution, most prominent in the superotemporal sector. Longitudinal analysis indicated a nonlinear trajectory of GCL loss, with accelerated decline in moderate OSA (P = 0.007) and relative stabilization in severe OSA. Each one-event-per-hour increase in ODI was associated with a 0.10 μm reduction in minimum GCL thickness (β = -0.10, 95% CI -0.17 to -0.02, P = 0.011).
Conclusions:
Among OSA-related nocturnal hypoxemia metrics, ODI showed the strongest associated with selective early GCL thinning, while RNFL changes are not detectable at this stage. These findings suggest that GCL could serve as a structural marker of subclinical neurodegeneration in OSA.
