Association between individual retinal layer thickness and visual acuity in patients with epiretinal membrane: a pilot study

Purpose We investigated the correlation between visual acuity (VA) and individual retinal layer thickness in the foveal, parafoveal, and perifoveal regions of patients with an idiopathic epiretinal membrane (ERM). Methods One hundred and five subjects presenting with unilateral idiopathic ERM were included in this study. We segmented each patient’s optical coherence tomography (OCT) image into seven layers and calculated the mean layer thickness in the foveal, parafoveal, and perifoveal regions using the Iowa Reference Algorithm. In 105 patients with ERM, we detected correlations between their macular regions’ individual retinal layer thickness and their best corrected VA. Thirty-one of the 105 patients with ERM underwent vitrectomy and completed six months of follow-up. We then compared the 31 surgical patients’ preoperative and postoperative individual retinal layer thickness in each macular region. Additionally, the association between preoperative individual retinal layer thickness in each macular region and VA six months post-surgery in patients with ≥ two Snellen lines of visual improvement was determined. Results Multiple linear regression analysis showed that the inner nuclear layer (INL) thickness in the foveal, parafoveal, and perifoveal region were all associated with VA in the 105 patients (R2 = 0.344, P < 0.001; R2 = 0.427, P < 0.001; and R2 = 0.340, P < 0.001, respectively). Thirty-one surgical patients 6 months post-surgery showed significantly decreased thicknesses (P ≤ 0.012) of the foveal INL, inner plexiform layer (IPL), and outer nuclear layer (ONL); the parafoveal retina nerve fiber layer (RNFL), IPL, INL, and ONL; and the perifoveal RNFL, IPL, INL, ganglion cell layer (GCL), outer plexiform layer (OPL), and photoreceptor layer (PRL). We found a weak correlation between postoperative VA and preoperative foveal and perifoveal RNFL thickness (r = 0.404 and r = 0.359, respectively), and a moderate correlation between postoperative VA and preoperative foveal and parafoveal INL thickness (r = 0.529 and r = 0.583, respectively) in the 31 surgical patients (P ≤ 0.047). The preoperative INL thickness in the foveal, parafoveal, and perifoveal regions showed a moderate to strong correlation (r = 0.507, 0.644, and 0.548, respectively), with postoperative VA in patients with ≥ 2 lines of visual improvement (P ≤ 0.038). Conclusion We detected a correlation between retinal damage and VA in the parafoveal, perifoveal, and foveal regions. Our results suggest that INL thickness in all macular regions may be a prognostic factor for postoperative VA in ERM patients

Alterations in Macular Microvasculature in Pterygium Patients Measured by OCT Angiography

Previous studies have reported an association between pterygia and maculopathy, yet the underlying mechanisms and alterations to the macular microvasculature in pterygium patients have yet to be fully elucidated. Our study conducted an analysis of macular superficial vessel length density (VLD) and vessel perfusion density (VPD) to establish associations between the conjunctival and macular microvasculature in patients with unilateral and bilateral pterygia. We revealed a loss of macular microvasculature in the outer nasal (ON) region in both unilateral and bilateral pterygium patients. VLD was significantly decreased in both pterygium groups in the ON region, and VPD was notably lower in bilateral pterygium patients in the same area. Furthermore, in unilateral pterygium patients, the vessel percent pixel coverage (PPC) of the pterygium and the area of the pterygium exhibited a negative correlation with VLD in the ON region. Multiple stepwise linear regression models indicated that the PPC could best predict VLP in the ON region. Taken together, our findings suggest that patients with pterygia may be more susceptible to macular diseases, and this may be due to a compensatory increase in blood perfusion via the anterior ciliary artery. These results underscore the importance of managing maculopathy in patients with pterygia

WNT-inhibitory factor 1-mediated glycolysis protects photoreceptor cells in diabetic retinopathy

Abstract Background In diabetic retinopathy (DR), hypoxia-inducible factor (HIF-1α) induces oxidative stress by upregulating glycolysis. This process leads to neurodegeneration, particularly photoreceptor cell damage, which further contributes to retinal microvascular deterioration. Further, the regulation of Wnt-inhibitory factor 1 (WIF1), a secreted Wnt signaling antagonist, has not been fully characterized in neurodegenerative eye diseases. We aimed to explore the impact of WIF1 on photoreceptor function within the context of DR. Method Twelve-week-old C57BL/KsJ-db/db mice were intravitreally injected with WIF1 overexpression lentivirus. After 4 weeks, optical coherence tomography (OCT), transmission electron microscopy (TEM), H&E staining, and electroretinography (ERG) were used to assess the retinal tissue and function. The potential mechanism of action of WIF1 in photoreceptor cells was explored using single-cell RNA sequencing. Under high-glucose conditions, 661 W cells were used as an in vitro DR model. WIF1-mediated signaling pathway components were assessed using quantitative real-time PCR, immunostaining, and western blotting. Result Typical diabetic manifestations were observed in db/db mice. Notably, the expression of WIF1 was decreased at the mRNA and protein levels. These pathological manifestations and visual function improved after WIF1 overexpression in db/db mice. TEM demonstrated that WIF1 restored damaged mitochondria, the Golgi apparatus, and photoreceptor outer segments. Moreover, ERG indicated the recovery of a-wave potential amplitude. Single-cell RNA sequencing and in vitro experiments suggested that WIF1 overexpression prevented the expression of glycolytic enzymes and lactate production by inhibiting the canonical Wnt signaling pathway, HIF-1α, and Glut1, thereby reducing retinal and cellular reactive oxygen species levels and maintaining 661 W cell viability. Conclusions WIF1 exerts an inhibitory effect on the Wnt/β-catenin-HIF-1α-Glut1 glycolytic pathway, thereby alleviating oxidative stress levels and mitigating pathological structural characteristics in retinal photoreceptor cells. This mechanism helps preserve the function of photoreceptor cells in DR and indicates that WIF1 holds promise as a potential therapeutic candidate for DR and other neurodegenerative ocular disorders. Graphical Abstrac