ReviewJournal of clinical medicine2026
The Pathophysiological Association Between Obstructive Sleep Apnea and Glaucoma: A Current Update.
Review in Journal of clinical medicine, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Glaucoma is a chronic, progressive optic neuropathy and the second leading cause of irreversible blindness worldwide. Although elevated intraocular pressure (IOP) remains the principal modifiable risk factor, it is neither necessary nor sufficient for disease development. The literature indicates that systemic conditions such as obstructive sleep apnea (OSA) may contribute to its pathogenesis. The pathophysiology of glaucoma is supported by several theories, primarily the mechanical and vascular theories. This review describes the pathophysiological links between OSA and glaucoma considering current theories. The principal connecting mechanism appears to be chronic intermittent hypoxia and reduced ocular perfusion pressure, which trigger optic nerve head hypoxia, oxidative stress, and biomechanical remodeling of the lamina cribrosa. These processes interact within a vicious cycle that progressively compromises the metabolic support of optic nerve axons. The mechanisms described are particularly relevant to normal-tension glaucoma, which may be associated with OSA. Retinal nerve fiber layer thinning appears among the earliest markers of optic nerve vulnerability, whereas IOP and visual field changes are more variable. These observations underscore the clinical relevance of the OSA-glaucoma relationship and support a multidisciplinary approach incorporating routine ophthalmic screening for subclinical optic nerve damage.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.