ReviewProgress in retinal and eye research2021
The vital role for nitric oxide in intraocular pressure homeostasis.
Review in Progress in retinal and eye research, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.
What it found
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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
46 citing papers in PubMed, 103 citations in OpenAlex.
- Nanoparticles in Vascular Dementia: Advantages and Challenges.CNS neuroscience & therapeutics · 2026Review
- Therapeutic Gases in Biomedicine: Updates on Nitric Oxide and Beyond.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Review
- Assessing systemic endothelial dysfunction in glaucoma subtypes and pseudoexfoliation using photoplethysmography-based flow mediated dilation.International ophthalmology · 2026Article
- Piezo1 Activates an Autocrine Angiopoietin-2-Integrin Signaling Loop in Schlemm's Canal to Regulate Intraocular Pressure.bioRxiv : the preprint server for biology · 2025Article
- TRPV4 activation by TGFβ2 enhances cellular contractility and drives ocular hypertension.eLife · 2025Article
- Identification and Validation of Key Biomarkers in the Proximal Aqueous Humor Outflow Pathway.Current issues in molecular biology · 2025Article
- Endothelial cell-specific postnatal deletion of Nos3 preserves intraocular pressure homeostasis via macrophage recruitment and NOS2 upregulation.The Journal of clinical investigation · 2025Article
- FYN regulates aqueous humor outflow and IOP through the phosphorylation of VE-CADHERIN.Nature communications · 2025Article
- Real-world impact of latanoprostene bunod ophthalmic solution 0.024% in glaucoma therapy: a narrative review.Frontiers in ophthalmology · 2025Review
- Mechanobiology in the eye.npj biological physics and mechanics · 2025Review
- GWAS-by-subtraction reveals an IOP-independent component of primary open angle glaucoma.Nature communications · 2024Article
- Effect of the Mediterranean Diet (MeDi) on the Progression of Retinal Disease: A Narrative Review.Nutrients · 2024Review
- The S341P mutant MYOC renders the trabecular meshwork sensitive to cyclic mechanical stretch.Heliyon · 2024Article
- Aging and intraocular pressure homeostasis in mice.Aging cell · 2024Article
- The Factors Affecting the Stability of IOP Homeostasis.Investigative ophthalmology & visual science · 2024Article
- Article
- Pathological Mechanism and Clinical Therapy Progress of Schlemm's Canal.Journal of ophthalmology · 2024Review
- Estrogen dysregulation, intraocular pressure, and glaucoma risk.Experimental eye research · 2023Review
- Development and testing of a metabolic chamber for effluent collection during whole eye perfusions.Experimental eye research · 2023Article
- Trabecular Meshwork Movement Controls Distal Valves and Chambers: New Glaucoma Medical and Surgical Targets.Journal of clinical medicine · 2023Review
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 2 countries.
Funding
Abstract
Catalyzed by endothelial nitric oxide (NO) synthase (eNOS) activity, NO is a gaseous signaling molecule maintaining endothelial and cardiovascular homeostasis. Principally, NO regulates the contractility of vascular smooth muscle cells and permeability of endothelial cells in response to either biochemical or biomechanical cues. In the conventional outflow pathway of the eye, the smooth muscle-like trabecular meshwork (TM) cells and Schlemm's canal (SC) endothelium control aqueous humor outflow resistance, and therefore intraocular pressure (IOP). The mechanisms by which outflow resistance is regulated are complicated, but NO appears to be a key player as enhancement or inhibition of NO signaling dramatically affects outflow function; and polymorphisms in NOS3, the gene that encodes eNOS modifies the relation between various environmental exposures and glaucoma. Based upon a comprehensive review of past foundational studies, we present a model whereby NO controls a feedback signaling loop in the conventional outflow pathway that is sensitive to changes in IOP and its oscillations. Thus, upon IOP elevation, the outflow pathway tissues distend, and the SC lumen narrows resulting in increased SC endothelial shear stress and stretch. In response, SC cells upregulate the production of NO, relaxing neighboring TM cells and increasing permeability of SC's inner wall. These IOP-dependent changes in the outflow pathway tissues reduce the resistance to aqueous humor drainage and lower IOP, which, in turn, diminishes the biomechanical signaling on SC. Similar to cardiovascular pathogenesis, dysregulation of the eNOS/NO system leads to dysfunctional outflow regulation and ocular hypertension, eventually resulting in primary open-angle glaucoma.
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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.