ReviewISRN ophthalmology2013
New therapeutic targets for intraocular pressure lowering.
Review in ISRN ophthalmology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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
16 citing papers in PubMed, 40 citations in OpenAlex.
- Ischemia-Induced Neurodegeneration in Glaucoma: Mechanistic Insights and Translational Opportunities for Psychoplastogen-Based Therapies.Pharmaceuticals (Basel, Switzerland) · 2026Review
- From a Fish Protein to a Novel Glaucoma Therapeutic: Stanniocalcin-1 for Intraocular Pressure Reduction.Advances in ophthalmology and optometry · 2025Article
- The endocannabinoid system and ophthalmic pathologies: a review of molecular mechanisms and its implications for clinical practice.Frontiers in medicine · 2025Review
- The Mirror Theory: Parallels between Open Angle and Angle Closure Glaucoma.Life (Basel, Switzerland) · 2024Review
- Paeoniflorin alleviates TGF-β2-mediated extracellular matrix remodeling and oxidative stress in human trabecular meshwork cells.International ophthalmology · 2024Article
- Therapeutic Potential of Cannabinoids in Glaucoma.Pharmaceuticals (Basel, Switzerland) · 2023Review
- Article
- The Role of miR-29 Family in TGF-β Driven Fibrosis in Glaucomatous Optic Neuropathy.International journal of molecular sciences · 2022Review
- Astragaloside IV Attenuates Ocular Hypertension in a Mouse Model of TGFβ2 Induced Primary Open Angle Glaucoma.International journal of molecular sciences · 2021Article
- Intraocular pressure-lowering effect ofInternational journal of medical sciences · 2021Article
- Substances of Interest That Support Glaucoma Therapy.Nutrients · 2019Review
- Latanoprostene bunod ophthalmic solution 0.024% for IOP lowering in glaucoma and ocular hypertension.Expert opinion on pharmacotherapy · 2017Review
- Cannabinoids increase mechanosensitivity of trigeminal ganglion neurons innervating the inner walls of rat anterior chambers via activation of TRPA1.Journal of Huazhong University of Science and Technology. Medical sciences = Hua zhong ke ji da xue xue bao. Yi xue Ying De wen ban = Huazhong keji daxue xuebao. Yixue Yingdewen ban · 2016Article
- Discovery of Molecular Therapeutics for Glaucoma: Challenges, Successes, and Promising Directions.Journal of medicinal chemistry · 2016Review
- Present and New Treatment Strategies in the Management of Glaucoma.The open ophthalmology journal · 2015Article
- Novel therapies for open-angle glaucoma.F1000prime reports · 2014Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Primary open-angle glaucoma (POAG) is a leading cause of irreversible and preventable blindness and ocular hypertension is the strongest known risk factor. With current classes of drugs, management of the disease focuses on lowering intraocular pressure (IOP). Despite of their use to modify the course of the disease, none of the current medications for POAG is able to reduce the IOP by more than 25%-30%. Also, some glaucoma patients show disease progression despite of the therapeutics. This paper examines the new described physiological targets for reducing the IOP. The main cause of elevated IOP in POAG is thought to be an increased outflow resistance via the pressure-dependent trabecular outflow system, so there is a crescent interest in increasing trabecular meshwork outflow by extracellular matrix remodeling and/or by modulation of contractility/TM cytoskeleton disruption. Modulation of new agents that act mainly on trabecular meshwork outflow may be the future hypotensive treatment for glaucoma patients. There are also other agents in which modulation may decrease aqueous humour production or increase uveoscleral outflow by different mechanisms from those drugs available for glaucoma treatment. Recently, a role for the ghrelin-GHSR system in the pathophysiology modulation of the anterior segment, particularly regarding glaucoma, has been proposed.
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.