ReviewJournal of ocular pharmacology and therapeutics : the official journal of the Association for Ocular Pharmacology and Therapeutics
The microfibril hypothesis of glaucoma: implications for treatment of elevated intraocular pressure.
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 33 papers.
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Who cites it
33 citing papers in PubMed, 51 citations in OpenAlex.
- Pro-Inflammatory Cytokines in Aqueous Humor From ADAMTS10-Mutant Beagles at an Early Stage of Open-Angle Glaucoma.Veterinary ophthalmology · 2026Article
- Fibrosis-Related Gene and Protein Expression in Normal and Glaucomatous Trabecular Meshwork Cells.Investigative ophthalmology & visual science · 2025Article
- Alterations in anterior lens capsule structure and LTBP-2 expression in primary angle-closure glaucoma.BMJ open ophthalmology · 2024Article
- Relative ability of aqueous humor from dogs with and without primary angle-closure glaucoma and ADAMTS10 open-angle glaucoma to catalyze or inhibit collagenolysis.Veterinary ophthalmology · 2024Article
- Exome-based mutation screening in South African children with primary congenital glaucoma.Eye (London, England) · 2023Article
- Pathogenesis of glaucoma: Extracellular matrix dysfunction in the trabecular meshwork-A review.Clinical & experimental ophthalmology · 2022Review
- Endogenous expression of Notch pathway molecules in human trabecular meshwork cells.Experimental eye research · 2022Article
- Thrombospondin-1 Signaling Through the Calreticulin/LDL Receptor Related Protein 1 Axis: Functions and Possible Roles in Glaucoma.Frontiers in cell and developmental biology · 2022Review
- Article
- GLIS1 regulates trabecular meshwork function and intraocular pressure and is associated with glaucoma in humans.Nature communications · 2021Article
- Integrating Network Pharmacology, Transcriptome and Artificial Intelligence for Investigating Into the Effect and Mechanism of Ning Fei Ping Xue Decoction Against the Acute Respiratory Distress Syndrome.Frontiers in pharmacology · 2021Article
- Increased Susceptibility to Glaucomatous Damage in Microfibril Deficient Mice.Investigative ophthalmology & visual science · 2020Article
- Scleral structure and biomechanics.Progress in retinal and eye research · 2020Review
- Update on Animal Models of Exfoliation Syndrome.Journal of glaucoma · 2018Review
- Aqueous outflow - A continuum from trabecular meshwork to episcleral veins.Progress in retinal and eye research · 2017Review
- Life under pressure: The role of ocular cribriform cells in preventing glaucoma.Experimental eye research · 2016Review
- Expanding the clinical spectrum of COL1A1 mutations in different forms of glaucoma.Orphanet journal of rare diseases · 2016Article
- Influence of Age on Ocular Biomechanical Properties in a Canine Glaucoma Model with ADAMTS10 Mutation.PloS one · 2016Article
- Article
- Functional Anatomy of the Outflow Facilities.The Veterinary clinics of North America. Small animal practice · 2015Review
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Microfibrils are macromolecular aggregates located in the extracellular matrix of both elastic and nonelastic tissues that have essential functions in formation of elastic fibers and control of signaling through the transforming growth factor beta (TGFβ) family of cytokines. Elevation of systemic TGFβ and chronic activation of TGFβ signal transduction are associated with diseases caused by mutations in microfibril-associated genes, including FBN1. A role for microfibrils in glaucoma is suggested by identification of risk alleles in LOXL1 for exfoliation glaucoma and mutations in LTBP2 for primary congenital glaucoma, both of which are microfibril-associated genes. Recent identification of a mutation in another microfibril-associated gene, ADAMTS10, in a dog model of primary open-angle glaucoma led us to form the microfibril hypothesis of glaucoma, which in general states that defective microfibrils may be an underlying cause of glaucoma. Microfibril defects could contribute to glaucoma through alterations in biomechanical properties of tissue and/or through effects on signaling through TGFβ, which is well established to be elevated in the aqueous humor of glaucoma patients. Recent work has shown that diseases caused by microfibril defects are associated with increased concentrations of TGFβ protein and chronic activation of TGFβ-mediated signal transduction. In analogy with other microfibril-related diseases, defective microfibrils could provide a mechanism for the elevation of TGFβ2 in glaucomatous aqueous humor. If glaucoma shares mechanisms with other diseases caused by defective microfibrils, such as Marfan syndrome, therapeutic interventions to inhibit chronic activation of TGFβ signaling used in those diseases may be applied to 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.