navigating-angles-retrospective-analysis-one-year-outcomes-gonioscopy

Navigating the Angles: A Retrospective Analysis of One-year Outcomes of Gonioscopy-assisted Transluminal Trabeculotomy in Primary Open-angle Glaucoma

This study aimed to evaluate postoperative angle changes following gonioscopy-assisted transluminal trabeculotomy (GATT) in patients with primary ...

Nanjing Tongren Hospital

Glaucoma is the main reason for irreversible blindness, and pathological increased intraocular pressure is the leading risk factor for glaucoma. It is reported that trabecular meshwork cell injury is closely associated with the elevated intraocular pressure. The current study aimed to investigate the role of small nucleolar RNA host gene 3 (SNHG3) in human trabecular meshwork (HTM) cells under oxidative stress. A series of experiments including real-time quantitative polymerase chain reaction, subcellular fractionation assay, western blot analysis, cell counting kit-8 assay, RNA pull down, flow cytometry analysis, and RNA immunoprecipitation assay were used to explore the biological function and regulatory mechanism of SNHG3 in HTM cells under oxidative stress. First, we observed that H O induced SNHG3 upregulation in HTM cells. Then, we found that SNHG3 silencing alleviated H O -induced oxidative damage in HTM cells. Moreover, snail family transcriptional repressor 2 (SNAI2) knockdown alleviated the oxidative damage induced by H O in HTM cells. Mechanistically, SNHG3 bound with ELAV like RNA binding protein 2 (ELAVL2) to stabilize SNAI2. Finally, SNAI2 overexpression counteracted the effect of SNHG3 silencing on H O -treated HTM cells. In conclusion, our results demonstrated that SNHG3 cooperated with ELAVL2 to modulate cell apoptosis and extracellular matrix accumulation by stabilizing SNAI2 in HTM cells under oxidative stress.

SNHG3 cooperates with ELAVL2 to modulate cell apoptosis and extracellular matrix accumulation by stabilizing SNAI2 in human trabecular meshwork cells under oxidative stress.

Myopia has raised a predominant public concern among minors. A recent genome-wide association study (GWAS) identified six novel loci in Asian adults. Whether these genetic loci works for myopia in minors remains unknown and worthy of exploration.

Genetic Association Study Revealed Three Loci Were Associated Risk of Myopia Among Minors.

There is accumulating evidence to suggest that microRNAs (miRNAs) are associated with the progressive optic neuropathy including glaucoma. Apoptosis of retinal ganglion cells (RGCs) is a hallmark of glaucoma. The present study focused on the effects of miR-145-5p on RGC apoptosis in glaucoma.

MicroRNA-145-5p targeting of TRIM2 mediates the apoptosis of retinal ganglion cells via the PI3K/AKT signaling pathway in glaucoma.

Trimetazidine (TMZ), as a metabolic regulator, has been widely testified to exhibit positive therapeutic effects on various disease models, but its role in diabetic retinopathy has not been reported. Therefore, this study was designed with the purpose of exploring the effects of TMZ on high-glucose (HG)-induced retinal endothelial dysfunction and its underlying mechanism. To establish DR model in vitro, 30 mM glucose was applied to induce human retinal endothelial cells (HRECs). Cell proliferation, invasion, and migration were examined by means of Cell Counting Kit-8, transwell, and wound healing assays, respectively. The tubule formation experiment was used to test the tubulogenesis ability and fluorescein isothiocyanate (FITC)-albumin was utilized to measure the permeability of monolayer HRECs. In addition, immunofluorescence and Western blot were employed to detect protein expression. Compared with the HG-induced group, TMZ concentration dependently inhibited the proliferation, migration, and angiogenesis of HG-induced HRECs, decreased the permeability of monolayer HRECs, and increased the protein expression levels of Claudin-5 and VE-cadherin. In addition, TMZ intervention increased the expression of p-PI3K, p-AKT, and p-mTOR but decreased the expression of LC3I, LC3II, and Beclin 1, which were then partially reversed by P13 K inhibitor (LY294002). Moreover, the autophagy agonist rapamycin (RAPA) was also testified to reverse the inhibitory effects of TMZ on the proliferation, migration, and angiogenesis of HG-induced HRECs. In summary, TMZ inhibited excessive autophagy by activating PI3K/Akt/mTOR pathway, thereby improving retinal endothelial dysfunction induced by HG.

Trimetazidine mitigates high glucose-induced retinal endothelial dysfunction by inhibiting PI3K/Akt/mTOR pathway-mediated autophagy.

Glaucoma is a progressive optic neuropathy and improper treatment may cause irreversible damage to visual function. Gastrodin is an effective active substance extracted from Gastrodia elata and possesses antioxidant as well as anti-inflammatory properties. However, the therapeutic potential of gastrodin for retinal ischemia/reperfusion (I/R) injury remains unclear. We adopted oxygen and glucose deprivation/reoxygenation (OGD/R) to induce R28 cells with the aim of simulating glaucomatous neurodegeneration. CCK-8 analysis and TUNEL were applied for examining cell proliferation and apoptosis . In addition, RT-qPCR and ELISA were performed to test the releases of inflammatory factors in cells . Related indicators of intracellular oxidative stress and ROS production were detected by corresponding kits. Moreover, western blot was applied to assay the expressions of PI3K/AKT/Nrf2 pathway-related proteins. OGD/R induction contributed to the decreased cell viability and reduced Bcl-2 protein expression, while the protein contents of Bax, Cyto-C, c-caspase 9 and c-PARP as well as ROS production were ascended. The co-treatment of hypoxia and gastrodin greatly improved R28 cell viability but effectively suppressed cell apoptosis, ROS level and the releases of OGD/R-induced inflammatory factors as well as oxidative stress. In addition, OGD/R stimulation reduced Nrf2, accompanied by a decrease in the phosphorylation levels of PI3K and AKT. Gastrodin significantly promoted the activation of PI3K/AKT/Nrf2 signaling pathway in R28 cells, which was then counteracted by PI3K/AKT inhibitors. In conclusion, the present study suggested that gastrodin has a protective effect on OGD/R-induced R28 cell injury, which is achieved through the activation of the PI3K/AKT/Nrf2 signaling pathway.

Gastrodin protects retinal ganglion cells from ischemic injury by activating phosphatidylinositol 3-kinase/protein kinase B/nuclear factor erythroid 2-related factor 2 (PI3K/AKT/Nrf2) signaling pathway.

Inflammation is involved in the development of myopia. n-3 polyunsaturated fatty acids (n-3 PUFAs) have vasodilating and anti-inflammatory effects, which may be involved in controlling myopia. It is of great significance to explore the relationship between n-3 PUFA intakes and juvenile myopia in order to control and alleviate myopia among teenagers through dietary intervention.

Association of n-3 polyunsaturated fatty acid intakes with juvenile myopia: A cross-sectional study based on the NHANES database.

Blue light poses a risk of retinal damage with excessive exposure. BlingLife-marigold extract (BLM) is an alcohol extract of magrigold, which contains abundant lutein, zeaxanthin and meso-zeaxanthin. This study aimed to explore the role and potential mechanisms of BLM in blue light-induced retinal damage both in vivo and in vitro. Rats or human retinal pigment epithelial cell line (ARPE-19) were exposed to blue LED light with or without BLM treatment. The retinal morphology changes of rat were evaluated by H&E staining. Mitochondrial morphology was examined by using a transmission electron microscope. Besides, mitochondria oxidative stress was evaluated by detecting mitochondrial membrane potential, ROS, MDA and SOD levels. By measuring γH2AX expression and performing SA-β-galactosidase (gal) staining, cell senescence was assessed. Additionally, cell cycle was detected using flow cytometry. Western blot was employed to examine the expression of NRF2 and HO-1. Results indicated that BLM could protect against blue light-induced damage of rat retinal tissues and ARPE-19 cells, as evidenced by the improved histopathological changes, alleviated mitochondria oxidative stress and attenuated senescence of tissues and cells. More importantly, BLM activated NRF2/HO-1 signaling, and addition of NRF2 inhibitor ML385 significantly blocked the protective effects of BLM on ARPE-19 cells exposed to blue light. In conclusion, BLM can provide an effective protection against blue light-induced retinal damage at least partly by activating NRF2/HO-1 signaling, suggesting that BLM may be useful for the prevention of blue light-induced retinal injury.

BlingLife-Marigold Extract Alleviates Blue Light-Induced Retinal Mitochondria Oxidative Stress and Senescence by Activating NRF2/HO-1 Signaling.

N6-methyladenosine (m6A), a pivotal RNA modification, has garnered considerable attention in cell biology and disease research. m6A plays a critical role in the regulation of gene expression, cell proliferation, differentiation, and apoptosis, with particular relevance to the onset and progression of ocular diseases. This review examines the current research on m6A in ocular diseases, including keratitis, cataracts, glaucoma, retinopathy, thyroid ophthalmopathy, and ocular tumors, highlighting its functional significance and potential mechanisms in these conditions. Recent studies suggest that m6A modification influences cellular fate and pathophysiological processes by modulating the expression of key genes. However, a deeper understanding of the precise mechanisms underlying m6A action in ocular diseases is still needed. By synthesizing the existing literature, this review seeks to offer novel insights and identify potential therapeutic targets, thereby advancing clinical applications for ocular disease treatment.

N6-methyladenosine: a key regulator in ocular disease mechanisms and treatment.

Ferroptosis, a recently discovered type of programmed cell death (PCD) distinguished by iron overload and lipid peroxidation, differs fundamentally from necrosis, apoptosis, and autophagy. Emerging evidence indicates that ferroptosis is deeply implicated in the disruption of the ocular microenvironment, wherein both structural and immune cells are significantly compromised. Rather than being an isolated cellular event, ferroptosis actively engages in a complex bidirectional crosstalk with the ocular immune system, driving neuroinflammation and tissue degeneration. In this review, we shift the paradigm from traditional disease-specific descriptions to the underlying microenvironmental interactions that dictate ocular health. Furthermore, we systematically evaluate the therapeutic potential of emerging interventions. Specifically, we highlight the latest breakthroughs in utilizing natural and dietary compounds as potent ferroptosis regulators. Crucially, we address current translational limitations by exploring advanced drug delivery systems, such as nanocarriers and hydrogels, designed to effectively overcome the blood-retinal barrier (BRB) and improve targeted efficacy. Ultimately, this review provides a comprehensive roadmap for advancing ferroptosis-targeted therapies from the laboratory to clinical ophthalmology.

Article	Year
SNHG3 cooperates with ELAVL2 to modulate cell apoptosis and extracellular matrix accumulation by stabilizing SNAI2 in human trabecular meshwork cells under oxidative stress. Environmental toxicology\| PubMed ID: 33522089	2021
Genetic Association Study Revealed Three Loci Were Associated Risk of Myopia Among Minors. Pharmacogenomics and personalized medicine\| PubMed ID: 34007202	2021
MicroRNA-145-5p targeting of TRIM2 mediates the apoptosis of retinal ganglion cells via the PI3K/AKT signaling pathway in glaucoma. The journal of gene medicine\| PubMed ID: 34291866	2021
Trimetazidine mitigates high glucose-induced retinal endothelial dysfunction by inhibiting PI3K/Akt/mTOR pathway-mediated autophagy. Bioengineered\| PubMed ID: 35259050	2022
Gastrodin protects retinal ganglion cells from ischemic injury by activating phosphatidylinositol 3-kinase/protein kinase B/nuclear factor erythroid 2-related factor 2 (PI3K/AKT/Nrf2) signal... Bioengineered\| PubMed ID: 35609324	2022
Association of n-3 polyunsaturated fatty acid intakes with juvenile myopia: A cross-sectional study based on the NHANES database. Frontiers in pediatrics\| PubMed ID: 37138572	2023
BlingLife-Marigold Extract Alleviates Blue Light-Induced Retinal Mitochondria Oxidative Stress and Senescence by Activating NRF2/HO-1 Signaling. Journal of microbiology and biotechnology\| PubMed ID: 40016150	2025
N6-methyladenosine: a key regulator in ocular disease mechanisms and treatment. Cell death discovery\| PubMed ID: 41315216	2025
Ferroptosis and the eye: bridging the gap between cell death and vision preservation. Frontiers in immunology\| PubMed ID: 41988183	2026

Qingsong Yang

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