ReviewClinical epigenetics2025
Epigenetics of glaucoma in the trabecular meshwork.
Review in Clinical epigenetics, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
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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
1 citing paper in PubMed.
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.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Glaucoma represents a predominant cause of irreversible blindness globally, characterized by the association of elevated intraocular pressure (IOP) and retinal ganglion cell loss with dysfunction of the trabecular meshwork (TM), the principal tissue regulating conventional aqueous humor outflow. Emerging evidence suggests that this dysfunction is not exclusively driven by genetic variation or mechanical stress; rather, it is significantly influenced by epigenetic mechanisms that integrate factors such as aging, hypoxia/oxidative stress, glucocorticoid exposure, and other environmental challenges into enduring alterations in TM phenotype. This review synthesizes current understanding of the primary epigenetic mechanisms involved in glaucomatous TM remodeling, encompassing DNA methylation, histone modifications, non-coding RNAs (including microRNAs and long non-coding RNAs), and RNA N⁶-methyladenosine (m⁶A) methylation. In this study, we elucidate the role of aberrant DNA methylation in the regulation of profibrotic genes, such as TGF-β1 and GDF7, elasticity-modifying genes like LOXL1, and repetitive elements, which collectively contribute to extracellular matrix (ECM) accumulation, tissue stiffening, and increased outflow resistance. Furthermore, we explore how dysregulated miRNA-lncRNA networks and histone acetylation/methylation influence central signaling pathways, including TGF-β/BMP-Smad, Wnt/β-catenin, RhoA/ROCK, PI3K-Akt, and NF-κB. These pathways are crucial in orchestrating trabecular meshwork (TM) fibrosis, cytoskeletal remodeling, cellular senescence, and impaired stress responses. Additionally, we investigate the emerging roles of m⁶A regulators, such as METTL3, YTHDF2, and YTHDC2, at the intersection of outflow pathway fibrosis and retinal ganglion cell vulnerability. We propose that epigenetic modifiers, ncRNA-based therapies, and partial epigenetic reprogramming could offer innovative, TM-targeted, and neuroprotective strategies beyond conventional IOP-lowering treatments. Collectively, our findings support an integrated model wherein diverse epigenetic modifications converge to produce a stereotypical glaucomatous TM phenotype, thereby presenting novel opportunities for mechanism-based diagnosis and therapeutic intervention in 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.