International journal of ophthalmology最新文献

Aim: To explore the neuroprotective effects of high mobility group box 2 (HMGB2) knockdown on retinal ganglion cells (RGCs) in the retinal ischemia-reperfusion injury (RIRI).

Methods: Oxygen-glucose deprivation (OGD)-injured RGCs from postnatal three-day C57BL/6 mice pups and high intraocular pressure (IOP)-induced RIRI mice were used as cellular and animal models of RIRI. The expression of HMGB2 in the retina of RIRI mice and OGD-injured RGCs was detected through reverse transcription-polymerase chain reaction (RT-qPCR) and Western blotting. The effects of HMGB2 silencing on the morphological changes, RGCs survival, and cell apoptosis in mouse retinal tissues were observed through H&E staining, immunofluorescence staining with RNA-binding protein with multiple splicing (RBPMS) antibody, and TUNEL staining, respectively. RGC viability and apoptosis were examined by CCK-8 and flow cytometry assays. The levels of proteins associated with NOD-like receptor thermal protein domain associated protein 3 (NLRP3)-mediated pyroptosis [NLRP3, Caspase-1, GSDMD-N, interleukin (IL)-1β, IL-18] in vivo and in vitro were measured by Western blotting.

Results: HMGB2 protein and NLRP3 were upregulated in the retina of RIRI mice and OGD-injured RGCs (P<0.001). The retina was edematous, accompanied by disorganized cell arrangement and decreased thickness of all layers, and obvious vacuoles in ganglion cell layer. HMGB2 silencing alleviated the reduction in total retinal thickness and the severity of retinal tissue damage as well as suppressed RGC loss and retinal cell apoptosis in RIRI mice. OGD-induced RGC apoptosis was ameliorated after downregulation of HMGB2 in vitro. Intravitreal injection of the AAV-sh-HMGB2 and si-HMGB2 resulted in significantly decrease of NLRP3, Caspase-1, GSDMD-N, IL-1β, and IL-18 protein levels in the retinal tissues of RIRI mice and OGD-injured RGCs, respectively (all P<0.001).

Conclusion: HMGB2 knockdown protects against RGC apoptosis and pyroptosis after RIRI through suppressing NLRP3 inflammasome activation.

Aim: To test the effect of autophagy on inflammatory damage resulting from oxidative stress in adult retinal pigment epithelial cell line (ARPE-19).

Methods: ARPE-19 cells were pretreated with 200 and 600 µmol/L hydrogen peroxide (H₂O₂) at various time intervals. The changes of cell morphology, cell viability, reactive oxygen species (ROS) level, autophagic activity, and the inflammatory cytokines (TNFα, IL-6, and TGFβ) were measured at baseline and after treatment with autophagy inducer rapamycin (Rapa) and suppressor wortmannin (Wort) or shATG5.

Results: The levels of ROS, cytokines (TNFα, IL-6, and TGFβ), and autophagic activity were significantly increased in ARPE-19 cells after pretreated with H₂O₂ (all P<0.05) and IL-10 was significantly decreased (P<0.05). By upregulating autophagy, Rapa significantly reduced oxidative stress-induced secretion of pro-inflammatory factors (TNFα and IL-6) and ROS (all P<0.05), yet elevated the production of TGFβ (P<0.05). In contrast, suppression of autophagy through Wort or ATG5 knockdown reduced cell viability, increased cell apoptotic rate, and exacerbated the generation of ROS and inflammatory cytokines (TNFα, IL-6, and TGFβ; all P<0.05).

Conclusion: Autophagy demonstrates a protective effect on ARPE-19 cell through mitigating oxidative damage and oxidative stress-induced inflammatory response. Regulation of autophagy may be a potential way for age-related macular degeneration.

Improvements in surgical techniques have led to 90% success in the surgical repair of rhegmatogenous retinal detachment (RRD). However, anatomical reattachment of the retina does not ensure complete recovery of visual function. The incidence of metamorphopsia remains the most common postoperative complaint, from 24% to 88.6%. Currently, the risk factors of metamorphopsia are categorized into macular involvement, retinal shift, outer retinal folds, subretinal fluid, secondary epiretinal membrane, outer retinal layer damage, and surgical approach. The associations of metamorphopsia with postoperative best-corrected visual acuity and postoperative vision-related quality of life were still controversial. The most popular methods for assessment of metamorphopsia remain the Amsler grid and M-Charts. Most treatments cannot progress beyond the management of negative visual sensations, through methods such as occlusion therapy and aniseikonia-correcting spectacles. The main treatment approach involves RRD prevention and the management of risk factors that can lead to postoperative metamorphopsia after RRD repair. Additional research concerning metamorphopsia treatment, further upgrades of auxiliary inspection methods, and more accurate microstructural assessments are needed to address this common complication.

Aim: To assess the relationship between dietary inflammatory index (DII) and prevalence of glaucoma among individuals aged 40y and above in the United States.

Methods: Participants were drawn from 2 cycles of the National Health and Nutrition Examination Survey (NHANES, 2005-2008) for a cross-sectional study. DII was calculated from 24-hour dietary recall questionnaire conducted by experienced researchers and data analyzed in R according to the NHANES user guide, "Stratified Multi-stage Probability Sampling". The relationship between DII and glaucoma was evaluated by multi-factor logistic regression analysis and the existence of a non-linear association examined by restricted cubic spline (RCS) analysis.

Results: A total of 5359 subjects were included and the cross-sectional analysis weighted to represent the US population of 109 million. DII was elevated in glaucoma patients (P<0.001) and smoking and alcohol use contributed to significant differences (P<0.001). DII correlated negatively with Healthy Eating Index (HEI)-2015 (Spearman rank correlation coefficient, r=-0.49). RCS analysis showed a linear relationship between DII and glaucoma risk (P of non-linear relationship =0.575).

Conclusion: An increased DII is strongly associated with high risk of glaucoma and diet-induced inflammation should be controlled to delay glaucoma progression.

Glaucoma is a group of diseases characterized by progressive optic nerve degeneration, with the characteristic pathological change being death of retinal ganglion cells (RGCs), which ultimately causes visual field loss and irreversible blindness. Elevated intraocular pressure (IOP) remains the most important risk factor for glaucoma, but the exact mechanism responsible for the death of RGCs is currently unknown. Neurotrophic factor deficiency, impaired mitochondrial structure and function, disrupted axonal transport, disturbed Ca²⁺ homeostasis, and activation of apoptotic and autophagic pathways play important roles in RGC death in glaucoma. This review was conducted using Web of Science, PubMed, Project, and other databases to summarize the relevant mechanisms of death of RGCs in glaucoma, in addition to outlining protective treatments to improve the degradation of RGCs.

Aim: To identify topographic determinants of the anterior chamber angle (ACA) in patients with keratoconus (KCN).

Methods: Four hundred and ten eyes of 294 patients with KCN were recruited for this study. First, complete ocular examinations were performed for all patients, including visual acuity measurement, refraction, and slit-lamp biomicroscopy. Then, all participants underwent corneal imaging by the Oculus Pentacam HR.

Results: The mean age of the participants was 32.40±8.52y (15-60y) and 69.5% of them were male. The mean ACA was 38.47°±5.75° (range: 14.40° to 56.50°) in the whole sample, 38.24°±6.00° in males, and 38.98°±5.11° in females (P=0.447). The mean ACA was significantly different among different groups of cone morphology, as patients with nipple cones showed the lowest mean ACA. Moreover, there were statistically significant differences in the mean ACA among different groups of cone locations, with patients having central cones exhibiting the lowest mean ACA (P<0.001). Anterior and posterior Q values were significantly, directly correlated with ACA (anterior Q: r=0.122, P=0.014, posterior Q: r=0.192, P<0.001).

Conclusion: This study provides critical insights into the risk factors for ACA narrowing in KCN patients, which is essential for planning intraocular surgeries. Patients with nipple and central cones exhibited the most significant ACA narrowing. Additionally, more negative Q-values are associated with increased ACA narrowing, highlighting the need for targeted diagnostic and therapeutic strategies.

Aim: To quantify and compare longitudinal thickness changes of the ganglion cell complex (GCC) and the choroid in patients with different patterns of age-related macular degeneration (AMD) progression.

Methods: Retrospective cohort analysis of anonymized data from participants aged 50y or more and diagnosed with early/intermediate AMD in at least one eye (with no evidence of advanced AMD). A total of 64 participants were included from the Instituto de Retina de Lisboa (IRL) study (IPL/2022/MetAllAMD_ESTeSL) and divided into 4 groups according to the Rotterdam classification for AMD. Spectral domain optical coherence tomography (SD-OCT) was used to assess and quantify GCC and choroid thickness at two time points (first visit vs last visit) with a minimum interval of 3y.

Results: In the GCC inner ring, a thinner thickness (P=0.001) was observed in the atrophic AMD group (51.3±21.4 µm) compared to the early AMD (84.3±11.5 µm), intermediate AMD (77.6±16.1 µm) and neovascular AMD (88.9±16.3 µm) groups. Choroidal thickness quantification showed a generalized reduction in the central circle (P=0.002) and inner ring (P=0.001). Slight reductions in retinal thickness were more accentuated in the inner ring in the atrophic AMD (-13%; P<0.01).

Conclusion: The variation of the analyzed structures could be an indicator of risk of progression with neurodegenerative (GCC) or vascular (choroid) pattern in the intermediate and atrophic AMD. The quantification of both structures can provide important information about the risk of disease progression in the early and intermediate stages but also for the evolution pattern into late stages (atrophic or neovascular).