ReviewJournal of ophthalmology2014
The role of epigenetics in the fibrotic processes associated with glaucoma.
Review in Journal of ophthalmology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 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
24 citing papers in PubMed, 43 citations in OpenAlex.
- Chromatin dynamics identifies 78 genes at loci associated with elevated intraocular pressure and primary open-angle glaucoma.bioRxiv : the preprint server for biology · 2026Article
- Epigenetics of glaucoma in the trabecular meshwork.Clinical epigenetics · 2025Review
- MicroRNA-29b targets ADAM12 and 19 to regulate the extracellular matrix in lamina cribrosa cells.Cell and tissue research · 2025Article
- Challenging glaucoma with emerging therapies: an overview of advancements against the silent thief of sight.Frontiers in medicine · 2025Review
- Epigenetics in Glaucoma.Medicina (Kaunas, Lithuania) · 2024Review
- Salivary Exosomes in Health and Disease: Future Prospects in the Eye.International journal of molecular sciences · 2023Review
- Ultrastructural analysis of explanted CyPass microstents and correlation with clinical findings.Graefe's archive for clinical and experimental ophthalmology = Albrecht von Graefes Archiv fur klinische und experimentelle Ophthalmologie · 2022Article
- HIF-1α aggravates pathologic myopia through the miR-150-5p/LAMA4/p38 MAPK signaling axis.Molecular and cellular biochemistry · 2022Article
- Article
- Molecular regulation of neuroinflammation in glaucoma: Current knowledge and the ongoing search for new treatment targets.Progress in retinal and eye research · 2022Review
- The role of Vitamin D3 in ocular fibrosis and its therapeutic potential for the glaucomatous trabecular meshwork.Frontiers in ophthalmology · 2022Review
- Fibrotic Changes to Schlemm's Canal Endothelial Cells in Glaucoma.International journal of molecular sciences · 2021Article
- Review
- A broad perspective on the molecular regulation of retinal ganglion cell degeneration in glaucoma.Progress in brain research · 2020Review
- The Pro-Fibrotic Behavior of Human Tenon's Capsule Fibroblasts in Medically Treated Glaucoma Patients.Clinical ophthalmology (Auckland, N.Z.) · 2020Article
- Aberrant DNA methylation of miRNAs in Fuchs endothelial corneal dystrophy.Scientific reports · 2019Article
- Clinical Role of Epigenetics and Network Analysis in Eye Diseases: A Translational Science Review.Journal of ophthalmology · 2019Review
- Working your SOCS off: The role of ASB10 and protein degradation pathways in glaucoma.Experimental eye research · 2017Review
- Epigenetics and Signaling Pathways in Glaucoma.BioMed research international · 2017Review
- Steroid-induced ocular hypertension/glaucoma: Focus on pharmacogenomics and implications for precision medicine.Progress in retinal and eye research · 2017Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Glaucoma is an optic neuropathy that affects 60 million people worldwide. The main risk factor for glaucoma is increased intraocular pressure (IOP), this is currently the only target for treatment of glaucoma. However, some patients show disease progression despite well-controlled IOP. Another possible therapeutic target is the extracellular matrix (ECM) changes in glaucoma. There is an accumulation of ECM in the lamina cribrosa (LC) and trabecular meshwork (TM) and upregulation of profibrotic factors such as transforming growth factor β (TGF β ), collagen1 α 1 (COL1A1), and α -smooth muscle actin ( α SMA). One method of regulating fibrosis is through epigenetics; the study of heritable changes in gene function caused by mechanisms other than changes in the underlying DNA sequence. Epigenetic mechanisms have been shown to drive renal and pulmonary fibrosis by upregulating profibrotic factors. Hypoxia alters epigenetic mechanisms through regulating the cell's response and there is a hypoxic environment in the LC and TM in glaucoma. This review looks at the role that hypoxia plays in inducing aberrant epigenetic mechanisms and the role these mechanisms play in inducing fibrosis. Evidence suggests that a hypoxic environment in glaucoma may induce aberrant epigenetic mechanisms that contribute to disease fibrosis. These may prove to be relevant therapeutic targets in glaucoma.
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.