ReviewJournal of ocular pharmacology and therapeutics : the official journal of the Association for Ocular Pharmacology and Therapeutics
Bioactive lysophospholipids: role in regulation of aqueous humor outflow and intraocular pressure in the context of pathobiology and therapy of glaucoma.
Review in Journal of ocular pharmacology and therapeutics : the official journal of the Association for Ocular Pharmacology and Therapeutics. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 27 citations in OpenAlex.
- Lipids and lipid regulators in intraocular pressure homeostasis.Current opinion in pharmacology · 2025Review
- The role of YAP/TAZ mechanosignaling in trabecular meshwork and Schlemm's canal cell dysfunction.Vision research · 2024Review
- Identification of the novel role of sterol regulatory element binding proteins (SREBPs) in mechanotransduction and intraocular pressure regulation.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2023Article
- Fibrotic Response of Human Trabecular Meshwork Cells to Transforming Growth Factor-Beta 3 and Autotaxin in Aqueous Humor.Biomolecules · 2022Article
- Multiomics analysis reveals the mechanical stress-dependent changes in trabecular meshwork cytoskeletal-extracellular matrix interactions.Frontiers in cell and developmental biology · 2022Article
- Critical Roles of Lysophospholipid Receptors in Activation of Neuroglia and Their Neuroinflammatory Responses.International journal of molecular sciences · 2021Review
- Crosstalk between transforming growth factor β-2 and Autotaxin in trabecular meshwork and different subtypes of glaucoma.Journal of biomedical science · 2021Article
- TRPV4 is activated by mechanical stimulation to induce prostaglandins release in trabecular meshwork, lowering intraocular pressure.PloS one · 2021Article
- Alteration in Lysophospholipids and Converting Enzymes in Glaucomatous Optic Nerves.Investigative ophthalmology & visual science · 2020Article
- Endogenous ocular lipids as potential modulators of intraocular pressure.Journal of cellular and molecular medicine · 2020Article
- Role of the autotaxin-lysophosphatidic acid axis in glaucoma, aqueous humor drainage and fibrogenic activity.Biochimica et biophysica acta. Molecular basis of disease · 2020Article
- Multi-Omics Approach for Studying Tears in Treatment-Naïve Glaucoma Patients.International journal of molecular sciences · 2019Article
- Lysophosphatidic Acid Induces ECM Production via Activation of the Mechanosensitive YAP/TAZ Transcriptional Pathway in Trabecular Meshwork Cells.Investigative ophthalmology & visual science · 2018Article
- Trabecular meshwork stiffness in glaucoma.Experimental eye research · 2017Review
- Unravelling the interplay of sphingolipids and TGF-β signaling in the human corneal stroma.PloS one · 2017Article
- Sphingolipids and ceramides of mouse aqueous humor: Comparative profiles from normotensive and hypertensive DBA/2J mice.Biochimie · 2014Article
- Cross-talk between ciliary epithelium and trabecular meshwork cells in-vitro: a new insight into glaucoma.PloS one · 2014Article
Corrections and comments
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Authors and funding
1 author at 1 institution in 1 country.
Funding
Abstract
Homeostasis of aqueous humor (AH) outflow and intraocular pressure (IOP) is essential for normal vision. Impaired AH outflow through the trabecular meshwork (TM) and a resultant elevation in IOP are common changes in primary open-angle glaucoma (POAG), which is the most prevalent form of glaucoma. Although elevated IOP has been recognized as a definitive risk factor for POAG and lowering elevated IOP remains a mainstay for glaucoma treatment, little is known about the molecular mechanisms, especially external cues and intracellular pathways, involved in the regulation of AH outflow in both normal and glaucomatous eyes. In addition, despite the recognition that increased resistance to AH outflow via the conventional pathway consisting of TM and Schlemm's canal is the main cause for elevated IOP, there are no clinically approved drugs that target the conventional pathway to lower IOP in glaucoma patients. The aim of this article is to briefly review published work on the importance of bioactive lysophospholipids (eg, lysophosphatidic acid and sphingosine-1-phosphate), their receptors, metabolism, signaling, and role in the regulation of AH outflow via the TM and IOP, and to discuss pharmacological targeting of key proteins in the lysophospholipid signaling pathways to lower IOP in glaucoma patients.
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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.