Glaucoma, a leading cause of irreversible blindness, is a complex polygenic disease where significant clinical and genetic heterogeneity do not explain all glaucoma cases, highlighting the need for a deeper understanding of molecular mechanisms like epigenetics. This review examines the emerging role of key epigenetic mechanisms, specifically DNA methylation, histone modifications, and non-coding RNAs in glaucoma pathogenesis and their potential as biomarkers and therapeutic targets. We discuss how aberrant DNA methylation (e.g., GDF7 hypomethylation/CDKN2B hypermethylation) promotes trabecular meshwork fibrosis and increases optic nerve vulnerability, contributing to disease development and/or progression. The METTL23 histone methylation linked to retinal ganglion cell death at normal eye pressure, and disease-specific microRNA profiles further support the role of epigenetic involvement in glaucoma. The proof-of-concept studies of GDF7 neutralization in primate models and the OSK-factor reprogramming in aged and glaucoma mice models, show that epigenetic changes are reversible and can restore visual functions. DNA methylation-based epigenetic clocks identify glaucoma as an accelerated molecular aging process. Although promising, the current evidences are largely preclinical and long-term human data are still lacking. Nonetheless, the inherent reversible nature of epigenetics offers significant translational potential. Methylation, epigenetic clocks, and circulating microRNA profiles could enable early, non-invasive biomarkers for diagnosis and prognosis. Future efforts are needed to validate biomarkers in large cohorts and develop targeted epigenetic therapies. In conclusion, epigenetics is redefining our current understanding of glaucoma from a pressure-based disease to a modifiable link between genes and environment paving the way for personalized care for vision preservation beyond pressure-lowering treatments.
biomarkersDNA methylationepigeneticsglaucomahistone modificationsneurodegenerationnon-coding RNAThe author(s) declared that financial support was received for this work and/or its publication. This work is supported by the King Saud University through the Vice Deanship of Scientific Research Chair and Glaucoma Research Chair in Ophthalmology (GRC-2026).section-at-acceptanceRNAIntroduction
Glaucoma is a group of optic neuropathies characterized by elevated intraocular pressure (IOP), progressive loss of retinal ganglion cells (RGCs), damage to the optic nerve, and blindness (Dietze et al., 2025; Weinreb et al., 2014). The estimated worldwide prevalence of adult-onset glaucoma is 3.5% in the population aged 40 years and above, affecting around 80 million people globally, with an estimated projection to nearly 112 million by 2040 (Allison et al., 2020; Tham et al., 2014; Al-Manjoumi et al., 2023). Since elevated IOP is considered a major risk factor for RGC death in glaucoma, the current clinical management is also focused on lowering IOP (Park et al., 2023). However, up to 40% or more of glaucoma patients do not exhibit high IOP but still suffer from progressive optic nerve damage, as seen in patients with normal-tension glaucoma (NTG) (Kim and Park, 2016). These cases demonstrate that there are several other non-IOP factors contributing to glaucoma development.
Glaucoma is a complex multifactorial disease involving both genetic and environmental influences (Wiggs, 2012). A number of genetic studies, including genome-wide, have identified several Mendelian genes (e.g., MYOC, CYP1B1, PAX6, FOXC1), chromosomal loci (GLC1A-P), and DNA variants associated with glaucoma (Kolovos et al., 2025; Tirendi et al., 2023; Zukerman et al., 2020; Abu-Amero et al., 2015). Although these studies have provided significant mechanistic insights into disease pathogenesis, they fail to explain the clinical variability seen in glaucoma onset, progression, and treatment response, suggesting the role of factors beyond genetic determinants (D’Esposito et al., 2024; Wang and Wang, 2023). There is evidence to believe that the environmental factors, such as aging, oxidative stress, and inflammation, interact with the genome in complex ways, inducing aberrant epigenetic regulation that might be the missing link, beyond the genetic determinants (Figure 1) (Wang and Wang, 2023; Dolinoy and Jirtle, 2008; Medeiros et al., 2025).
Conceptual model of epigenetics as the link between genetics and environment in the complex pathogenesis of glaucoma. Environmental factors interact with the genetic blueprint, and epigenetic mechanisms process these signals to regulate and influence crucial pathological outcomes, including extracellular matrix (ECM) remodeling, fibrosis, oxidative stress, trabecular meshwork (TM) dysfunction, intraocular pressure (IOP) alteration, leading to retinal ganglion cell (RGC) death and the eventual clinical manifestation of glaucoma.
Flowchart shows environmental factors and genetic factors impacting epigenetic factors, which modulate cellular events in the eye such as ECM remodeling, fibrosis, oxidative stress, TM dysfunction, IOP, and RGC death leading to glaucoma.
Epigenetics refers to the heritable changes observed in gene expression without alteration in the DNA sequence (Kachhawaha et al., 2023). There is strong evidence to suggest that epigenetics might be associated with glaucoma development and progression, plausibly by altering gene expression profiles critical to IOP control, optic nerve integrity, and neuroinflammation. These biological processes are central to aqueous humor dynamics, RGC survival, immune responses, and extracellular matrix (ECM) remodeling, which are strongly implicated in glaucoma (Figure 1) (D’Esposito et al., 2024; Tonti et al., 2024).
Eye represents an excellent model for epigenetic research (Alkozi et al., 2017; Lanza et al., 2019). The purpose of this review is to examine the epigenetic contributions of DNA methylation, histone modifications, N6-methyladenosine (m6A) methylation, and non-coding RNAs in glaucoma pathogenesis and their clinical translational potential.
Epigenetic mechanisms in glaucomaDNA methylation
DNA methylation is often referred to as ‘the epigenetic switch.’ It involves the addition of a methyl group to a cytosine base, prominently at CpG sites near gene promoters, causing gene silencing when hypermethylated or gene transcription when hypomethylated (Jin and Liu, 2018; Lim and Maher, 2010). Methylation is a tightly regulated process involving specific enzymes that are critical for developmental processes, cellular differentiation, and maintenance of genomic stability. These include the ‘writers’ and ‘maintainers,’ which are the DNA Methyltransferases (DNMTs), like DNMT1 for maintenance and DNMT3A/B for new establishment. The “erasers” are the Ten-Eleven Translocation (TET) enzymes, which control the on/off switch by oxidizing the methyl group (Dan and Chen, 2022). DNA methylation offers a dynamic interface between environmental stimuli (e.g., oxidative stress) and gene expression in ocular tissues. Aberrant expression of these enzymes can lead to abnormal methylation patterns and dysregulation of genes involved in key processes implicated in glaucoma pathogenesis, such as ECM remodeling, oxidative stress, and neurodegeneration (Bou Ghanem et al., 2024; Fernández-Albarral et al., 2024).
Evidence of differential DNA methylation in glaucoma
Several studies have demonstrated aberrant DNA methylation in different types of glaucoma. Junemann et al. reported a significantly higher global DNA methylation in blood cells of POAG patients compared to controls and PXG patients (Junemann et al., 2014). The trabeculectomy sections from glaucomatous eyes were reported to have significant DNA hypomethylation of Alu repetitive elements in POAG and PACG, and significant DNA hypermethylation of HERV-K in POAG patients (Chansangpetch et al., 2018). These methylation changes were proposed to predispose the trabecular meshwork (TM) cells to a profibrotic phenotype (Chansangpetch et al., 2018).
In PXG, the LOXL1 promoter is reported to be hypermethylated in lens capsule and human Tenon fibroblasts that correlated with reduced LOXL1 expression and increased ECM cross-linking (Greene et al., 2020; Ye et al., 2015). Interestingly, treatment of human Tenon Fibroblasts with DNMT inhibitor, 5-aza-dC, restored LOXL1 expression in PXG fibroblasts (Greene et al., 2020). Conversely, Kapuganti et al. reported hypomethylation of the clusterin promoter in patients with PXG (Kapuganti et al., 2023). In another study, CDKN2B gene promoter hypermethylation at the 9p21 locus has been linked to NTG susceptibility in women (Burdon et al., 2018). CDKN2B silencing due to hypermethylaiton causes its suppression that may increase the optic nerve’s vulnerability to non-IOP stressors (Burdon et al., 2018). This study elegantly demonstrated how epigenetic errors through aberrant methylation can impact critical RGC survival pathways, leading to neurodegeneration even at normal IOP.
Mechanistic evidence of DNA methylation in glaucoma
High IOP is the result of decreased outflow capacity at the level of the TM and Schlemm’s canal, the primary exit route of aqueous humor (Carreon et al., 2017). Dexamethasone (DEX)-treated primary human TM cells exhibited hypomethylation of the thrombospondin-1 (THBS1) promoter region and reduced transcript levels of 2 DNA methyltransferases (DNMTs), DNMT1 and DNMT3A (Choy et al., 2025). This change was consistent with DNA methylation inhibitors, 5-azacytosine (5-AC) or 5-aza-2′-deoxycytidine (5-aza-dC), inducing an increase in THBS1 protein levels, leading to the reduced outflow facility ex vivo and increased IOP in vivo adult male C57BL/6 J mice (Choy et al., 2025). These results highlight a clear mechanism in which DNMT downregulation and promoter hypomethylation alter THBS1 expression and influence ECM composition and aqueous outflow resistance. In glaucoma, fibrosis is one of the key mechanisms in glaucoma development and progression, as a result of ECM deposition in the TM at the anterior of the eye, and at the optic nerve head in the lamina cribrosa, leading to aqueous outflow resistance, elevated IOP, and subsequently glaucoma (Keller and Peters, 2022). The GDF7 gene promoter region is aberrantly hypomethylated in glaucomatous TM samples and TET-dependent (Wan et al., 2021). Hypomethylation causes gene activation, which releases the brake, causing GDF7 protein overexpression, increasing proteins like α-SMA, promoting fibrosis which clogs the drainage pathway, raising IOP. This landmark study is a prime example of a targetable epigenetic mechanism in POAG. Crucially, in a therapeutic proof-of-concept, neutralizing GDF7 with antibodies reduced this fibrosis and improved outflow in a primate model. This study showed that GDF7 is a direct, reversible, and therapeutic targetable epigenetic cause of high IOP and fibrosis in POAG, offering a potential for a novel anti-fibrotic therapy (Wan et al., 2021). Likewise, glaucomatous Schlemm’s canal endothelial cells have been shown to exhibit distinct methylation profiles in genes (TGFBR3, TBX3, TNXB1, DAXX, and PITX2) enriched in pathways regulating outflow resistance. However, further studies are needed to validate these findings (Cai et al., 2020).
Taken together, these studies suggest a complex and gene-specific methylation landscape in glaucoma subtypes and illustrate how DNA methylation can act as a molecular switch modulating distinct cellular pathways, promoting ECM remodeling in PXG (via LOXL1 or CLU) and influencing neuroprotective cell-cycle regulation in NTG (via CDKN2B), thereby contributing directly to disease susceptibility. It can thus be speculated that promoter methylation changes may represent potential blood-based biomarkers for glaucoma risk assessment and gender-specific susceptibility, as well as a valuable target for new treatments to mitigate glaucoma or fibrosis-related outflow resistance to restore normal TM function and outflow facility.
Epigenetic reprogramming
In vivo epigenetic reprogramming using Yamanaka OSK factors (Oct4, Sox2, Klf4) has shown promise in preclinical models. Reprogramming aged or glaucomatous RGCs reverses DNA methylation patterns to a youthful state, restoring a healthy transcriptome and visual function in mice. Transient OSK expression in glaucomatous eyes reversed vision loss in mice. The effect was dependent on DNA demethylases TET1 and TET2 (Lu et al., 2020). Moving beyond the initial proof-of-concept, a follow-up study provided compelling evidence of long-term safety and efficacy for vision recovery in glaucoma (Karg et al., 2023). The studies provide groundbreaking evidence of epigenetic reprogramming as a viable and sustainable approach for recovering lost vision in glaucoma with direct neural rescue and repair, moving us closer to a future where we can complement IOP-lowering.
DNA methylation-based EpiScores
Recent evidence suggests that DNA methylation (DNAm)-based EpiScores and GrimAge acceleration are positively associated with glaucoma risk, indicating that the disease may represent an accelerated molecular aging process (Medeiros et al., 2025; Jiang et al., 2025). EpiScore and GrimAge are epigenetic clock that predicts biological age and mortality risk based on DNAm patterns. Accelerated epigenetic aging compared to chronological aging is associated with a 15% higher odds of faster glaucoma progression. Importantly, this relationship remains strong even in patients with relatively low IOP, indicating that epigenetic aging may predispose the optic nerve to damage from things like oxidative stress, independent of IOP level (Medeiros et al., 2025). These results highlight the potential clinical importance of epigenetic age acceleration as a non-invasive predictor of progression.
Histone modifications
Histone modifications, including acetylation, methylation, phosphorylation, and ubiquitination, can regulate gene expression by altering chromatin structure (Davie and Chadee, 1998; Zhang et al., 2015). These modifications, catalyzed by specific enzymes, play significant roles in regulating genes involved in maintenance of IOP and RGC health, thereby influencing glaucoma risk and severity (Tonti et al., 2024; Feng et al., 2023).
Studies on glaucoma-related histone modifications have mainly focused on deacetylation (Pelzel et al., 2010; Schmitt et al., 2014; Alsarraf et al., 2014; Sharma et al., 2016). Histone deacetylation functions as a crucial epigenetic switch that may accelerate glaucomatous neurodegeneration (Pelzel et al., 2010; Sharma et al., 2016; Biermann et al., 2011). The HDAC inhibitors have consistently demonstrated to exhibit neuroprotective effects and improved surgical outcomes in different animal models of glaucoma, highlighting their potential utility as pharmacological agents in glaucoma (Feng et al., 2023; Schmitt et al., 2014; Alsarraf et al., 2014; Sharma et al., 2016; Biermann et al., 2011).
Histone methylation is another critical regulatory mechanism in glaucoma. The trimethylation mark H3K27me3, catalyzed by EZH2 are both detected in RGCs (Rao et al., 2012). A study by Rao et al. (2010) showed that inhibition of EZH2 induces RGC apoptosis, underscoring the essential role of EZH2-mediated H3K27me3 in retinal neuronal survival and suggesting its involvement in glaucomatous degeneration (Rao et al., 2010).
METTL23 and NTG: a histone methylation connection
Mutations in the METTL23 gene encoding a histone arginine methyltransferase have been linked to NTG (Pan et al., 2022). METTL23 catalyzes the dimethylation of H3R17 in the retina. The c.A23G mutation inherited as an autosomal dominant condition results in METTL23 loss of function, leading to impaired dimethylation of histone H3R17. This disrupts gene regulation in RGCs, causing RGC apoptosis through NF-κB signaling. The study highlights a novel epigenetic etiology in NTG and provides a direct evidence linking abnormal histone methylation to glaucomatous neurodegeneration (Pan et al., 2022; Scheetz et al., 2024; Liu and Sun, 2022). In addition, the findings open new therapeutic avenues to target the downstream inflammatory NF-κB signaling or the histone methylation modulators, shifting the paradigm beyond the conventional IOP-based approach of glaucoma management.
N6-methyladenosine (m6A) modification
m6A is a common mRNA modification regulating RNA stability, splicing, translation, and decay, affecting gene expression (Jiang et al., 2021; Patil et al., 2018). The modification involves regulation by writers (e.g., methyltransferase-like protein 3, METTL3), erasers (e.g., fat mass and obesity-associated, FTO), and readers (e.g., YTH family protein YTHDC2) (Jiang et al., 2021). These writer, eraser, and reader proteins play a significant role in various diseases, but are less studied in glaucoma.
In PXG, elevated global m6A levels and upregulated writer and reader enzymes (e.g., METTL3, YTHDC2) in aqueous humor may serve as biomarkers, with m6A-modified transcripts enriched in matrix organization pathways (D’Esposito et al., 2024; Guan et al., 2023). In another study, differential m6A-methylated lncRNAs in PXG aqueous humor influenced glaucoma-related genes and processes (Guan et al., 2024). In POAG, bioinformatics analyses identified differentially expressed m6A regulators (e.g., upregulated reader YTHDF1, downregulated reader YTHDC2) in TM tissues. Silencing YTHDC2 in human TM cells enhanced migration and ECM synthesis, demonstrating a functional role in outflow resistance (Zhang et al., 2025). Current studies suggest that targeting writer and reader pathways could lead to new treatments. For example, blocking the writer METTL3 might control fibrosis in PXG, and silencing readers like YTHDC2 may prevent TM dysfunction in POAG (Tonti et al., 2024; Guan et al., 2024; Zhang et al., 2025).
To enhance clinical utility and highlight the diagnostic potential of the epigenetic changes discussed in the above sections, a summary of the key markers characterized by their subtype-specific roles in POAG, PXG, and NTG is listed in Table 1.
Summary of key subtype-specific epigenetic markers in glaucoma.
Noncoding RNAs (ncRNAs) like microRNAs (miRNAs), long non-coding RNAs (lncRNAs), and circular RNAs (circRNAs) are pivotal players in cell regulatory networks across a broad spectrum of biological processes implicated in glaucoma (Rong et al., 2021; Costa et al., 2025). Differential expression and abnormal function of these regulatory molecules can affect gene networks related to fibrosis, IOP, and optic nerve health, making them promising biomarker candidates and drug targets (Rong et al., 2021; Zhang et al., 2021; Huang et al., 2022).
MiRNAs
miRNAs are the most extensively studied class of ncRNAs in glaucoma and have been elegantly reviewed elsewhere for detailed molecular summaries (Dobrzycka et al., 2023; Greene et al., 2022; Martinez and Peplow, 2022). Several studies have confirmed that these small RNA molecules (∼19–23 nucleotides in length) regulate a wide range of pathological processes, including ECM remodeling, TM cell function, RGC apoptosis, and oxidative stress.
In the TM, multiple miRNAs (e.g., miR-29b and miR-200a) exert anti-fibrotic effects by targeting pathways like TGF-β and Wnt/β-catenin to counteract ECM accumulation (Keller and Peters, 2022; Luna et al., 2009; Luna et al., 2011; Luna et al., 2012; Yu et al., 2022). miRNAs such as miR-143/145 and miR-200c regulate TM cell contractility and IOP, with knockout studies demonstrating reduced IOP and improved outflow in mice (Luna et al., 2012; Li et al., 2017). Others, including miR-18a-5p, also target TGF-β2 signaling to reduce contractility and fibrosis (Knox et al., 2022). Beyond IOP regulation, miRNAs like miR-182, miR-100, and miR-96 influence RGC survival and offer neuroprotection (Kong et al., 2014; Li et al., 2019; Wang and Li, 2014), while others such as miR-27a modulate oxidative stress and inflammatory responses (Tabak et al., 2021).
miRNAs in ocular fluids show promise as biomarkers. Profiles in aqueous humor and plasma are disease-specific, aiding in subtype differentiation (Drewry et al., 2018; Hindle et al., 2019; Rao et al., 2020; Raga-Cervera et al., 2021; Tanaka et al., 2014; Kosior-Jarecka et al., 2021). For example, specific miRNAs like miR-125b-5p are differentially expressed in POAG versus PXG (Drewry et al., 2018). A plasma panel of miR-637, miR-1306-5p, and miR-3159 identified glaucoma patients with an AUC of 0.91 (Hindle et al., 2019), and serum miR-210-3p is elevated in POAG (Liu et al., 2019; Zhao et al., 2023). In addition, tear-based miRNAs have shown promise as a non-invasive method for glaucoma screening (Raga-Cervera et al., 2021). Moreover, miRNAs identified in aqueous humor (e.g., miR-143-3p, miR-125b-5p, and miR-1260b) have been proposed to serve as drug targets (Martinez and Peplow, 2022; Zhang et al., 2023). The functional roles and diagnostic potential of key identified miRNAs are summarized in Table 2.
Functional roles and differential expression of specific miRNAs in glaucoma.
LncRNAs are transcripts over 200 nucleotides that often act as miRNA sponges (Mattick et al., 2023). By impairing the biological activity of miRNAs, lncRNAs increase the production of proteins from the target mRNAs and their dysregulation is implicated in glaucoma. Key lncRNAs like MALAT1, ANRIL (also known as CDKN2B-AS1), and others (ENST00000552367 and NR_038379) influence TM cell proliferation, ECM remodeling, and RGC vulnerability (Burdon et al., 2018; Zhang et al., 2021; Huang et al., 2022; Pasquale et al., 2013). Xie et al. (2019) suggested that lncRNAs T267384, ENST00000607393, and T342877 might be potential therapy biomarkers for POAG. Some, including NR003923, H19, and LINC00028 are prospective targets for preventing post-surgical fibrosis (Yu et al., 2022; Zhu et al., 2020; Zhao et al., 2019; Sui et al., 2020). However, the functions and associated mechanisms of the role of most lncRNAs in glaucoma are not completely clear yet.
CircRNAs
Similarly, circRNAs are closed-loop molecules that sequester miRNAs to regulate gene expression (Wawrzyniak et al., 2018). A recent study demonstrated that the circRNA ZRANB1 is expressed in glial cells and it negatively regulates miR-217, promoting Müller cell proliferation and RGC apoptosis (Wang et al., 2018). The expression of cZRANB1 was upregulated in glaucoma-induced retinal degeneration, and its knockdown provided a protective effect by reducing retinal gliosis and RGC apoptosis. This effect was reversed by overexpression of RUNX2 (Wang et al., 2018). Targeting this cZRANB1/miR-217/RUNX2 network has neuroprotective potential (Wang et al., 2018). Recent research has identified some candidate circRNAs in ocular hypertension glaucoma models by high-throughput sequencing (Chen et al., 2020); however, the role of most circRNAs in glaucoma remains to be elucidated (Choudhari et al., 2025).
Translational and clinical potential
The epigenetic mechanisms discussed in this review have significant translational and clinical potential to improve glaucoma diagnosis, prognosis, and treatment (Figure 2). Epigenetic aging derived from blood samples (EpiScore) could serve as non-invasive biomarkers of disease susceptibility (Medeiros et al., 2025). Likewise, DNA methylation profiles (e.g., hypermethylation of LOXL1 in PXG or CDKN2B in NTG) and circulating miRNA panels in aqueous humor, tears, or plasma may enable early detection and differentiation between glaucoma subtypes (Greene et al., 2020; Burdon et al., 2018; Martinez and Peplow, 2022). The inherent reversible nature of epigenetic modifications makes them attractive drug targets for clinical intervention. For instance, the epigenetic reprogramming of RGCs using the OSK approach could be the future paradigm for glaucoma treatment to promote RGC survival and restore vision (Lu et al., 2020; Karg et al., 2023). Similarly, with the demonstrated proof-of-concept, GDF7 neutralization might emerge as a promising anti-fibrotic therapy in glaucoma (Wan et al., 2021). In addition, the development of key epigenetic enzyme inhibitors (e.g., DNMT or HDAC inhibitors) and RNA-based therapies (miRNA antagonists) may precisely rectify dysregulated glaucoma pathways in the TM and retina, to reduce fibrosis, lower IOP, and protect the RGCs.
Translational and clinical potential of epigenetics in glaucoma. Schematic representation of the pathways through which epigenetic research is transitioning from mechanistic insight to clinical application, highlighting opportunities in diagnostics, therapeutics, and personalized care.
Three-section infographic summarizes advances in glaucoma: diagnostic potential highlights blood-based epigenetic clocks, DNA methylation signatures, and miRNA panels; therapeutic opportunities note reversible epigenetics, OSK, GDF7, DNMT/TET, and miRNA mimics; personalized care emphasizes integrating genetic and epigenetic profiling for subtype-specific biomarkers and therapies. Summary boxes below reinforce non-invasive biomarkers, drug targets, and methylation profiles for subtype-specific treatment.Challenges and future perspectives
Despite the exciting avenues of epigenetics, there exist several challenges to effectively translate the potential of epigenetics to patient care. The current evidence is mostly based on preclinical and small-scale human studies, highlighting the need to validate the diagnostic and prognostic potential of biomarkers like EpiScore, DNA methylations, and miRNA panels in a diverse population-based longitudinal cohorts. To address these challenges, future research must utilize longitudinal studies and Mendelian randomization to ascertain whether these epigenetic marks are a primary drivers of glaucoma or are secondary consequences of the disease process and cellular stress. Integrating multi-omics data (genomics, epigenomics, and transcriptomics) will be essential to validate these markers as causative agents of disease progression. Furthermore, the high degree of tissue-specific origins of epigenetic changes also presents a significant problem. Consequently, mechanistic studies are required to determine if these changes in accessible samples, such as blood or tears, accurately reflect localized changes in the TM or the optic nerve.
Development of advanced ocular drug delivery systems, such as nanoparticle-based eye drops or viral vectors for CRISPR-based epigenetic editing, is highly crucial for safe and effective application of epigenetic modulators (e.g., OSK factors, GDF7, DNMT/HDAC inhibitors, miRNA mimics). Additionally, studies to investigate the effect of environmental factors like diet, exercise, and lifestyle on the ocular epigenetics would be vital steps towards preventative medicine. The ultimate goal will be to incorporate validated genetic and epigenetic data with routine clinical markers, such as IOP, visual fields, and optical coherence tomography, to pave the way for personalized medicine in glaucoma.
Conclusion
In conclusion, epigenetics redefines our understanding of glaucoma from a static pressure disorder to a modifiable disease at the interface of genetics and environment. Although there are challenges in terms of validation, causality, and drug delivery, the reversible nature of epigenetic mechanisms provides a powerful therapeutic opportunity. Future studies are needed to address these limitations to utilize epigenetics as a source of novel biomarkers, specific drug targets, and personalized care strategies to prevent vision loss beyond IOP control alone.
Author contributions
AK: Writing – original draft, Supervision, Conceptualization, Writing – review and editing. TS: Writing – review and editing, Data curation. TA: Writing – review and editing, Data curation. SA-O: Resources, Writing – review and editing, Conceptualization.
Acknowledgements
The authors would like to express their appreciation to Al-Sheikh Ibrahim Al-Sultan for his valuable support.
Conflict of interest
The author(s) declared that this work was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
Generative AI statement
The author(s) declared that generative AI was not used in the creation of this manuscript.
Any alternative text (alt text) provided alongside figures in this article has been generated by Frontiers with the support of artificial intelligence and reasonable efforts have been made to ensure accuracy, including review by the authors wherever possible. If you identify any issues, please contact us.
Publisher’s note
All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers. Any product that may be evaluated in this article, or claim that may be made by its manufacturer, is not guaranteed or endorsed by the publisher.
ReferencesAbu-AmeroK.KondkarA. A.ChalamK. V. (2015). An updated review on the genetics of primary open angle glaucoma. Int. J. Mol. Sci.16, 28886–28911. 10.3390/ijms16122613526690118Al-ManjoumiA. M.FilimbanM. A.BantanM. S.AbualhamayelH. A.YouldashO. A. (2023). Prevalence of risk factors among patients with glaucoma in jeddah, Saudi Arabia. Cureus15, e37689. 10.7759/cureus.3768937206536AlkoziH. A.FrancoR.PintorJ. J. (2017). Epigenetics in the eye: an overview of the Most relevant ocular diseases. Front. Genet.8, 144. 10.3389/fgene.2017.0014429075285AllisonK.PatelD.AlabiO. (2020). Epidemiology of glaucoma: the past, present, and predictions for the future. Cureus12, e11686. 10.7759/cureus.1168633391921AlsarrafO.FanJ.DahroujM.ChouC. J.YatesP. W.CrossonC. E. (2014). Acetylation preserves retinal ganglion cell structure and function in a chronic model of ocular hypertension. Investig. Ophthalmol. Vis. Sci.55, 7486–7493. 10.1167/iovs.14-1479225358731BiermannJ.BoyleJ.PielenA.LagrèzeW. A. (2011). Histone deacetylase inhibitors sodium butyrate and valproic acid delay spontaneous cell death in purified rat retinal ganglion cells. Mol. Vis.17, 395–403.21311741Bou GhanemG. O.WarehamL. K.CalkinsD. J. (2024). Addressing neurodegeneration in glaucoma: mechanisms, challenges, and treatments. Prog. Retin. Eye Res.100, 101261. 10.1016/j.preteyeres.2024.10126138527623BurdonK. P.AwadallaM. S.MitchellP.WangJ. J.WhiteA.KeaneM. C. (2018). DNA methylation at the 9p21 glaucoma susceptibility locus is associated with normal-tension glaucoma. Ophthalmic Genet.39, 221–227. 10.1080/13816810.2017.141365929265947CaiJ.DrewryM. D.PerkumasK.DismukeW. M.HauserM. A.StamerW. D. (2020). Differential DNA methylation patterns in human Schlemm’s canal endothelial cells with glaucoma. Mol. Vis.26, 483–493.32606567CarreonT.van der MerweE.FellmanR. L.JohnstoneM.BhattacharyaS. K. (2017). Aqueous outflow - a continuum from trabecular meshwork to episcleral veins. Prog. Retin. Eye Res.57, 108–133. 10.1016/j.preteyeres.2016.12.00428028002ChansangpetchS.PrombhulS.TantiseviV.SodsaiP.ManassakornA.HirankarnN. (2018). DNA methylation status of the interspersed repetitive sequences for LINE-1, alu, HERV-E, and HERV-K in trabeculectomy specimens from glaucoma eyes. J. Ophthalmol.2018, 9171536. 10.1155/2018/917153629651348ChenX.ZhouR.ShanK.SunY.YanB.SunX. (2020). Circular RNA expression profiling identifies glaucoma-related circular RNAs in various chronic ocular hypertension rat models. Front. Genet.11, 556712. 10.3389/fgene.2020.55671233133146ChoudhariJ. K.VeraJ.ChatterjeeT. (2025). A network biology-guided investigation of the long noncoding RNAs’ role in glaucoma. Methods Mol. Biol. Clifton N. J.2883, 427–453. 10.1007/978-1-0716-4290-0_1939702720ChoyK. Y.YangW.LingC.LiK.LiH. L.LungH. (2025). Hypomethylation of thrombospondin-1 promoter region is associated with reduced aqueous humor flow. Commun. Biol.8, 1430. 10.1038/s42003-025-08833-y41053513CostaS.La RoccaG.CavalieriV. (2025). Epigenetic regulation of chromatin functions by MicroRNAs and long noncoding RNAs and implications in human diseases. Biomedicines13, 725. 10.3390/biomedicines1303072540149701DanJ.ChenT. (2022). Genetic studies on mammalian DNA methyltransferases. Adv. Exp. Med. Biol.1389, 111–136. 10.1007/978-3-031-11454-0_536350508DavieJ. R.ChadeeD. N. (1998). Regulation and regulatory parameters of histone modifications. J. Cell. Biochem. Suppl.72 (30–31), 203–213. 10.1002/(SICI)1097-4644(1998)72:30/31+<203::AID-JCB25>3.0.CO;2-429345837DietzeJ.BlairK.ZeppieriM.HavensS. J. (2025). “Glaucoma,” in StatPearls. Treasure Island (FL): StatPearls Publishing. Available online at: http://www.ncbi.nlm.nih.gov/books/NBK538217/(Accessed May 7, 2025).DobrzyckaM.SulewskaA.BiecekP.CharkiewiczR.KarabowiczP.CharkiewiczA. (2023). miRNA studies in glaucoma: a comprehensive review of current knowledge and future perspectives. Int. J. Mol. Sci.24, 14699. 10.3390/ijms24191469937834147DolinoyD. C.JirtleR. L. (2008). Environmental epigenomics in human health and disease. Environ. Mol. Mutagen.49, 4–8. 10.1002/em.2036618172876DrewryM. D.ChallaP.KuchteyJ. G.NavarroI.HelwaI.HuY. (2018). Differentially expressed microRNAs in the aqueous humor of patients with exfoliation glaucoma or primary open-angle glaucoma. Hum. Mol. Genet.27, 1263–1275. 10.1093/hmg/ddy04029401312D’EspositoF.GaglianoC.BloomP. A.CordeiroM. F.AvitabileA.GaglianoG. (2024). Epigenetics in glaucoma. Med. Mex.60, 905. 10.3390/medicina60060905FengL.WangC.ZhangC.ZhangW.SongW. (2023). Role of epigenetic regulation in glaucoma. Biomed. Pharmacother.168, 115633. 10.1016/j.biopha.2023.11563337806089Fernández-AlbarralJ. A.RamírezA. I.de HozR.MatamorosJ. A.Salobrar-GarcíaE.Elvira-HurtadoL. (2024). Glaucoma: from pathogenic mechanisms to retinal glial cell response to damage. Front. Cell. Neurosci.18. 10.3389/fncel.2024.135456938333055GreeneA. G.EiversS. B.McDonnellF.DervanE. W. J.O’BrienC. J.WallaceD. M. (2020). Differential lysyl oxidase like 1 expression in pseudoexfoliation glaucoma is orchestrated via DNA methylation. Exp. Eye Res.201, 108349. 10.1016/j.exer.2020.10834933188817GreeneK. M.StamerW. D.LiuY. (2022). The role of microRNAs in glaucoma. Exp. Eye Res.215, 108909. 10.1016/j.exer.2021.10890934968473GuanJ.LiZ.WumaierA.MaY.XieL.WuH. (2023). Critical role of transcriptome-wide m6A methylation in the aqueous humor of patients with pseudoexfoliation glaucoma. Exp. Eye Res.231, 109473. 10.1016/j.exer.2023.10947337061115GuanJ.ChenX.LiZ.DengS.WumaierA.MaY. (2024). Role of N6-methyladenosine-related lncRnas in pseudoexfoliation glaucoma. Epigenetics19, 2348840. 10.1080/15592294.2024.234884038716769HindleA. G.ThoonenR.JasienJ. V.GrangeR. M. H.AminK.WiseJ. (2019). Identification of candidate miRNA biomarkers for glaucoma. Investig. Ophthalmol. Vis. Sci.60, 134–146. 10.1167/iovs.18-2487830629727HuangG.LiangD.LuoL.LanC.LuoC.XuH. (2022). Significance of the lncRNAs MALAT1 and ANRIL in occurrence and development of glaucoma. J. Clin. Lab. Anal.36, e24215. 10.1002/jcla.2421535028972JiangX.LiuB.NieZ.DuanL.XiongQ.JinZ. (2021). The role of m6A modification in the biological functions and diseases. Signal Transduct. Target Ther.6, 74. 10.1038/s41392-020-00450-x33611339JiangX.MahrooO. A.KhawajaA. P.Skowronska-KrawczykD.MackeyD. A.WiggsJ. L. (2025). Identification of blood-derived DNA methylation biomarkers of glaucoma and intraocular pressure measurements in three European ancestry cohorts including the Canadian longitudinal study on aging. Epigenetics20, 2566496. 10.1080/15592294.2025.256649641105805JinZ.LiuY. (2018). DNA methylation in human diseases. Genes. Dis.5, 1–8. 10.1016/j.gendis.2018.01.00230258928JunemannA. G. M.LenzB.ReulbachU.Schlotzer-SchrehardtU.RejdakR.BleichS. (2014). Genomic (epigenetic) DNA methylation in patients with open-angle glaucoma. Investig. Ophthalmol. Vis. Sci.55, 3809. 10.1111/j.1755-3768.2009.2242.xKachhawahaA. S.MishraS.TiwariA. K. (2023). Epigenetic control of heredity. Prog. Mol. Biol. Transl. Sci.198, 25–60. 10.1016/bs.pmbts.2023.03.00637225323KapugantiR. S.SahooL.MohantyP. P.HayatB.ParijaS.AloneD. P. (2023). Role of clusterin gene 3’-UTR polymorphisms and promoter hypomethylation in the pathogenesis of pseudoexfoliation syndrome and pseudoexfoliation glaucoma. Biochim. Biophys. Acta Gene Regul. Mech.1866, 194980. 10.1016/j.bbagrm.2023.19498037652361KargM. M.LuY. R.RefaianN.CameronJ.HoffmannE.HoppeC. (2023). Sustained vision recovery by OSK gene therapy in a mouse model of glaucoma. Cell. Reprogr.25, 288–299. 10.1089/cell.2023.007438060815KellerK. E.PetersD. M. (2022). Pathogenesis of glaucoma: extracellular matrix dysfunction in the trabecular meshwork‐a review. Clin. Exp. Ophthalmol.50, 163–182. 10.1111/ceo.1402735037377KimK. E.ParkK.-H. (2016). Update on the prevalence, etiology, diagnosis, and monitoring of normal-tension glaucoma. Asia-Pac J. Ophthalmol. Phila Pa5, 23–31. 10.1097/APO.000000000000017726886116KnoxJ.Bou-GhariosG.HamillK. J.WilloughbyC. E. (2022). MiR-18a-5p targets connective tissue growth factor expression and inhibits transforming growth factor β2-Induced trabecular meshwork cell contractility. Genes.13, 1500. 10.3390/genes1308150036011411KolovosA.MaxwellG.SouzeauE.CraigJ. E. (2025). Progress in translating glaucoma genetics into the clinic: a review. Clin. Exp. Ophthalmol.53, 246–259. 10.1111/ceo.1450039929609KongN.LuX.LiB. (2014). Downregulation of microRNA-100 protects apoptosis and promotes neuronal growth in retinal ganglion cells. BMC Mol. Biol.15, 25. 10.1186/s12867-014-0025-125406880Kosior-JareckaE.CzopM.GasińskaK.Wróbel-DudzińskaD.ZalewskiD. P.Bogucka-KockaA. (2021). MicroRNAs in the aqueous humor of patients with different types of glaucoma. Graefes Arch. Clin. Exp. Ophthalmol.259, 2337–2349. 10.1007/s00417-021-05214-z33929592LanzaM.BenincasaG.CostaD.NapoliC. (2019). Clinical role of epigenetics and network analysis in eye diseases: a translational science review. J. Ophthalmol.2019, 2424956. 10.1155/2019/242495631976085LiX.ZhaoF.XinM.LiG.LunaC.LiG. (2017). Regulation of intraocular pressure by microRNA cluster miR-143/145. Sci. Rep.7, 915. 10.1038/s41598-017-01003-z28424493LiX.WangQ.RenY.WangX.ChengH.YangH. (2019). Tetramethylpyrazine protects retinal ganglion cells against H2O2-induced damage via the microRNA-182/mitochondrial pathway. Int. J. Mol. Med.44, 503–512. 10.3892/ijmm.2019.421431173163LimD. H. K.MaherE. R. (2010). DNA methylation: a form of epigenetic control of gene expression. Obstet. Gynaecol.12, 37–42. 10.1576/toag.12.1.037.27556LiuW. W.SunY. (2022). Epigenetics in glaucoma: a link between DNA methylation and neurodegeneration. J. Clin. Investig.132, e163670. 10.1172/JCI16367036317630LiuY.WangY.ChenY.FangX.WenT.XiaoM. (2019). Discovery and validation of circulating Hsa-miR-210-3p as a potential biomarker for primary open-angle glaucoma. Investig. Ophthalmol. Vis. Sci.60, 2925–2934. 10.1167/iovs.19-2666331284309LuY.BrommerB.TianX.KrishnanA.MeerM.WangC. (2020). Reprogramming to recover youthful epigenetic information and restore vision. Nature588, 124–129. 10.1038/s41586-020-2975-433268865LunaC.LiG.QiuJ.EpsteinD. L.GonzalezP. (2009). Role of miR-29b on the regulation of the extracellular matrix in human trabecular meshwork cells under chronic oxidative stress. Mol. Vis.15, 2488–2497.19956414LunaC.LiG.QiuJ.EpsteinD. L.GonzalezP. (2011). Cross-talk between miR-29 and transforming growth factor-betas in trabecular meshwork cells. Investig. Ophthalmol. Vis. Sci.52, 3567–3572. 10.1167/iovs.10-644821273536LunaC.LiG.HuangJ.QiuJ.WuJ.YuanF. (2012). Regulation of trabecular meshwork cell contraction and intraocular pressure by miR-200c. PLOS ONE7, e51688. 10.1371/journal.pone.005168823272142MartinezB.PeplowP. V. (2022). MicroRNAs as biomarkers in glaucoma and potential therapeutic targets. Neural Regen. Res.17, 2368–2375. 10.4103/1673-5374.33898935535873MattickJ. S.AmaralP. P.CarninciP.CarpenterS.ChangH. Y.ChenL.-L. (2023). Long non-coding RNAs: definitions, functions, challenges and recommendations. Nat. Rev. Mol. Cell. Biol.24, 430–447. 10.1038/s41580-022-00566-836596869MedeirosF. A.VarmaA.JammalA. A.TsengH.ScottW. K. (2025). Accelerated epigenetic aging is associated with faster glaucoma progression: a DNA methylation study. Ophthalmology132, 550–560. 10.1016/j.ophtha.2024.12.03439716635PanY.SugaA.KimuraI.KimuraC.MinegishiY.NakayamaM. (2022). METTL23 mutation alters histone H3R17 methylation in normal-tension glaucoma. J. Clin. Investig.132, e153589. 10.1172/JCI15358936099048ParkJ.RittiphairojT.WangX.EJ.-Y.BicketA. K. (2023). Device-modified trabeculectomy for glaucoma. Cochrane Database Syst. Rev.3, CD010472. 10.1002/14651858.CD010472.pub336912740PasqualeL. R.LoomisS. J.KangJ. H.YaspanB. L.AbdrabouW.BudenzD. L. (2013). CDKN2B-AS1 genotype-glaucoma feature correlations in primary open-angle glaucoma patients from the United States. Am. J. Ophthalmol.155, 342–353.e5. 10.1016/j.ajo.2012.07.02323111177PatilD. P.PickeringB. F.JaffreyS. R. (2018). Reading m6A in the transcriptome: M6A-binding proteins. Trends Cell. Biol.28, 113–127. 10.1016/j.tcb.2017.10.00129103884PelzelH. R.SchlampC. L.NickellsR. W. (2010). Histone H4 deacetylation plays a critical role in early gene silencing during neuronal apoptosis. BMC Neurosci.11, 62. 10.1186/1471-2202-11-6220504333Raga-CerveraJ.BolarinJ. M.MillanJ. M.Garcia-MedinaJ. J.PedrolaL.Abellán-AbenzaJ. (2021). miRNAs and genes involved in the interplay between ocular hypertension and primary open-angle glaucoma. Oxidative stress, inflammation, and apoptosis networks. J. Clin. Med.10, 2227. 10.3390/jcm1011222734063878RaoR. C.TchedreK. T.MalikM. T. A.ColemanN.FangY.MarquezV. E. (2010). Dynamic patterns of histone lysine methylation in the developing retina. Investig. Ophthalmol. Vis. Sci.51, 6784–6792. 10.1167/iovs.09-473020671280RaoR. C.HennigA. K.MalikM. T. A.ChenD. F.ChenS. (2012). Epigenetic regulation of retinal development and disease. J. Ocul. Biol. Dis. Infor.4, 121–136. 10.1007/s12177-012-9083-023538488RaoA.ChakrabortyM.RoyA.SahayP.PradhanA.RajN. (2020). Differential miRNA expression: signature for glaucoma in pseudoexfoliation. Clin. Ophthalmol. Auckl N. Z.14, 3025–3038. 10.2147/OPTH.S25450433116354RongR.WangM.YouM.LiH.XiaX.JiD. (2021). Pathogenesis and prospects for therapeutic clinical application of noncoding RNAs in glaucoma: systematic perspectives. J. Cell. Physiol.236, 7097–7116. 10.1002/jcp.3034733634475ScheetzT. E.TollefsonM. R.RoosB. R.BoeseE. A.PouwA. E.StoneE. M. (2024). METTL23 variants and patients with normal-tension glaucoma. JAMA Ophthalmol.142, 1037–1045. 10.1001/jamaophthalmol.2024.382939325437SchmittH. M.PelzelH. R.SchlampC. L.NickellsR. W. (2014). Histone deacetylase 3 (HDAC3) plays an important role in retinal ganglion cell death after acute optic nerve injury. Mol. Neurodegener.9, 39. 10.1186/1750-1326-9-3925261965SharmaA.AnumanthanG.ReyesM.ChenH.BrubakerJ. W.SiddiquiS. (2016). Epigenetic modification prevents excessive wound healing and scar formation after glaucoma filtration surgery. Investig. Ophthalmol. Vis. Sci.57, 3381–3389. 10.1167/iovs.15-1875027367506SuiH.FanS.LiuW.LiY.ZhangX.DuY. (2020). LINC00028 regulates the development of TGFβ1-treated human tenon capsule fibroblasts by targeting miR-204-5p. Biochem. Biophys. Res. Commun.525, 197–203. 10.1016/j.bbrc.2020.01.09632085895TabakS.Schreiber-AvissarS.Beit-YannaiE. (2021). Crosstalk between MicroRNA and oxidative stress in primary open-angle glaucoma. Int. J. Mol. Sci.22, 2421. 10.3390/ijms2205242133670885TanakaY.TsudaS.KunikataH.SatoJ.KokubunT.YasudaM. (2014). Profiles of extracellular miRNAs in the aqueous humor of glaucoma patients assessed with a microarray system. Sci. Rep.4, 5089. 10.1038/srep0508924867291ThamY.-C.LiX.WongT. Y.QuigleyH. A.AungT.ChengC.-Y. (2014). Global prevalence of glaucoma and projections of glaucoma burden through 2040: a systematic review and meta-analysis. Ophthalmology121, 2081–2090. 10.1016/j.ophtha.2014.05.01324974815TirendiS.DomenicottiC.BassiA. M.VernazzaS. (2023). Genetics and glaucoma: the state of the art. Front. Med.10, 1289952. 10.3389/fmed.2023.128995238152303TontiE.Dell’OmoR.FilippelliM.SpadeaL.SalatiC.GaglianoC. (2024). Exploring epigenetic modifications as potential biomarkers and therapeutic targets in glaucoma. Int. J. Mol. Sci.25, 2822. 10.3390/ijms2505282238474069WanP.LongE.LiZ.ZhuY.SuW.ZhuoY. (2021). TET-Dependent GDF7 hypomethylation impairs aqueous humor outflow and serves as a potential therapeutic target in glaucoma. Mol. Ther. J. Am. Soc. Gene Ther.29, 1639–1657. 10.1016/j.ymthe.2020.12.03033388417WangS.LiK. (2014). MicroRNA-96 regulates RGC-5 cell growth through caspase-dependent apoptosis. Int. J. Clin. Exp. Med.7, 3694–3702.25419419WangW.WangH. (2023). Understanding the complex genetics and molecular mechanisms underlying glaucoma. Mol. Asp. Med.94, 101220. 10.1016/j.mam.2023.10122037856931WangJ.-J.ShanK.LiuB.-H.LiuC.ZhouR.-M.LiX.-M. (2018). Targeting circular RNA-ZRANB1 for therapeutic intervention in retinal neurodegeneration. Cell. Death Dis.9, 540. 10.1038/s41419-018-0597-729748605WawrzyniakO.ZarębskaŻ.RolleK.Gotz-WięckowskaA. (2018). Circular and long non-coding RNAs and their role in ophthalmologic diseases. Acta Biochim. Pol.65, 497–508. 10.18388/abp.2018_263930428483WeinrebR. N.AungT.MedeirosF. A. (2014). The pathophysiology and treatment of glaucoma: a review. Jama311, 1901–1911. 10.1001/jama.2014.319224825645WiggsJ. L. (2012). The cell and molecular biology of complex forms of glaucoma: updates on genetic, environmental, and epigenetic risk factors. Investig. Ophthalmol. Vis. Sci.53, 2467–2469. 10.1167/iovs.12-9483e22562842XieL.MaoM.WangC.ZhangL.PanZ.ShiJ. (2019). Potential biomarkers for primary open-angle glaucoma identified by long noncoding RNA profiling in the aqueous humor. Am. J. Pathol.189, 739–752. 10.1016/j.ajpath.2018.12.01130677397YeH.JiangY.JingQ.LiD.MaimaitiT.KasimuD. (2015). LOXL1 hypermethylation in pseudoexfoliation syndrome in the uighur population. Investig. Ophthalmol. Vis. Sci.56, 5838–5843. 10.1167/iovs.15-1661826348632YuS.TamA. L. C.CampbellR.RenwickN. (2022). Emerging evidence of noncoding RNAs in bleb scarring after glaucoma filtration surgery. Cells11, 1301. 10.3390/cells1108130135455980ZhangT.CooperS.BrockdorffN. (2015). The interplay of histone modifications - writers that read. EMBO Rep.16, 1467–1481. 10.15252/embr.20154094526474904ZhangF.ZhaoY.CaoM.JiaX.PanZ.ZhouD. (2021). The potential role of long noncoding RNAs in primary open-angle glaucoma. Graefes Arch. Clin. Exp. Ophthalmol.259, 3805–3814. 10.1007/s00417-021-05279-w34244823ZhangR.TaoY.HuangJ. (2023). The application of MicroRNAs in glaucoma research: a bibliometric and visualized analysis. Int. J. Mol. Sci.24, 15377. 10.3390/ijms24201537737895056ZhangH.GaoD.LiZ.AghayantsS.WuY.LiuZ. (2025). Epigenetic orchestration of RNA m6A methylation in wound healing and post-wound events. Int. J. Biol. Sci.21, 4927–4941. 10.7150/ijbs.11498840860194ZhaoY.ZhangF.PanZ.LuoH.LiuK.DuanX. (2019). LncRNA NR_003923 promotes cell proliferation, migration, fibrosis, and autophagy via the miR-760/miR-215-3p/IL22RA1 axis in human Tenon’s capsule fibroblasts. Cell. Death Dis.10, 594. 10.1038/s41419-019-1829-131391457ZhaoS.FangL.YanC.WeiJ.SongD.XuC. (2023). MicroRNA-210-3p mediates trabecular meshwork extracellular matrix accumulation and ocular hypertension - implication for novel glaucoma therapy. Exp. Eye Res.227, 109350. 10.1016/j.exer.2022.10935036566010ZhuH.DaiL.LiX.ZhangZ.LiuY.QuanF. (2020). Role of the long noncoding RNA H19 in TGF-β1-induced Tenon’s capsule fibroblast proliferation and extracellular matrix deposition. Exp. Cell. Res.387, 111802. 10.1016/j.yexcr.2019.11180231877306ZukermanR.HarrisA.VercellinA. V.SieskyB.PasqualeL. R.CiullaT. A. (2020). Molecular genetics of glaucoma: subtype and ethnicity considerations. Genes.12, 55. 10.3390/genes1201005533396423
Edited by:Xiaoyan Liu, National Institutes of Health (NIH), United States
Reviewed by:Lokesh Verma, Sanjeev Agrawal Global Educational, India