ReviewIndian journal of ophthalmology2023
Ion channels in dry eye disease.
Review in Indian journal of ophthalmology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 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
15 citing papers in PubMed, 17 citations in OpenAlex.
- Motugivatrep (SJP-0132) 0.3% Ophthalmic Suspension for Dry Eye Disease: A Randomized, Double-Masked, Placebo-Controlled, Multicenter, Phase 3 Trial.Clinical ophthalmology (Auckland, N.Z.) · 2026Trial
- Immune inflammatory targets and anti-inflammatory therapy in dry eye disease.International ophthalmology · 2026Review
- Distinct Tear Element Signatures in Primary Acquired Nasolacrimal Duct Obstruction Identified by Particle-Induced X-Ray Emission.Investigative ophthalmology & visual science · 2026Article
- Ionomic profiling of vitreous humor and serum in rhegmatogenous retinal detachment.Scientific reports · 2026Article
- Could the Phenotypic Outcomes of Genetic Variability in Cells Operating in Mechanically Dynamic Environments be Influenced by a Disrupted "Cell-ECM" Relationship? Using Cystic Fibrosis and Marfan Syndrome as an Example.BioEssays : news and reviews in molecular, cellular and developmental biology · 2026Review
- Current and Developing Therapeutics for Dry Eye Disease: Targeting Ion Channels.Current issues in molecular biology · 2026Review
- Molecular landscape connecting complications of dry eye disease: mechanisms, therapeutic targets, biomarkers, and future innovations.International ophthalmology · 2026Review
- Mesenchymal stem cell-derived extracellular vesicles for dry eye disease: principles, progress, and challenges.Extracellular vesicles and circulating nucleic acids · 2026Review
- Association between hot spring residency and dry eye disease: a crossover gene-environment interaction (GxE) study in Taiwan.Human genomics · 2025Article
- Article
- Evaluation of the Performance of an Ocular Surface Modulator Containing ST-Lysyal Versus Hyaluronic Acid Eyedrops in Patients with Dry Eye Disease: A Pilot Study.Ophthalmology and therapy · 2025Article
- Molecular Mechanisms Responsible for Mesenchymal Stem Cell-Dependent Attenuation of Tear Hyperosmolarity and Immune Cell-Driven Inflammation in the Eyes of Patients with Dry Eye Disease.Diseases (Basel, Switzerland) · 2024Review
- Calcium-sensing receptor (CaSR) modulates ocular surface chloride transport and its inhibition promotes ocular surface hydration.The ocular surface · 2024Article
- A Novel Quaternary Ammonium N-Propylamiodarone Bromide Provides Long-Lasting Analgesia Against Corneal Pain.Drug design, development and therapy · 2024Article
- Review
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 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Dry eye disease (DED) which affects millions of people worldwide is an ocular surface disease that is strongly associated with pain, discomfort, and visual disturbances. Altered tear film dynamics, hyperosmolarity, ocular surface inflammation, and neurosensory abnormalities are the key contributors to DED pathogenesis. The presence of discordance between signs and symptoms of DED in patients and refractoriness to current therapies in some patients underpin the need for studying additional contributors that can be modulated. The presence of electrolytes or ions including sodium, potassium, chloride, bicarbonate, calcium, and magnesium in the tear fluid and ocular surface cells contribute to ocular surface homeostasis. Ionic or electrolyte imbalance and osmotic imbalance have been observed in DED and feed-forward interaction between ionic imbalances and inflammation alter cellular processes in the ocular surface resulting in DED. Ionic balances in various cellular and intercellular compartments are maintained by dynamic transport via ion channel proteins present in cell membranes. Hence, alterations in the expression and/or activity of about 33 types of ion channels that belong to voltage-gated channels, ligand-gated channels, mechanosensitive ion channel, aquaporins, chloride ion channel, sodium-potassium-chloride pumps or cotransporters have been investigated in the context of ocular surface health and DED in animal and/or human subjects. An increase in the expression or activity of TRPA1, TRPV1, Nav1.8, KCNJ6, ASIC1, ASIC3, P2X, P2Y, and NMDA receptor have been implicated in DED pathogenesis, whereas an increase in the expression or activity of TRPM8, GABA
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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.