SODAS: Second-order optimization differential architecture search for diabetic retinopathy prediction.

Elevated expression of hsa_circ_0053004 in peripheral blood mononuclear cells correlates with endothelial dysfunction in diabetic retinopathy.

Rewiring the regulated cell death network in diabetic retinopathy: natural products as system-level modulators.

Background: Diabetic retinopathy is a complication of type 2 diabetes mellitus and arises due to vascular endothelial growth factor-A (VEGF-A), which promotes pathological retinal angiogenesis. Objective: To evaluate the association of VEGF single nucleotide polymorphisms with predisposition to proliferative diabetic retinopathy. Methodology: The study was conducted at Najaf Teaching Hospital, Iraq, from April 2023 to February 2024, and included 120 participants divided into three groups. Serum VEGF-A levels were measured to ascertain the genotype of two VEGF-A SNPs, rs6921438 and rs955772463. Results: the result show a progressive rise in VEGF-A across all the groups: mean value of 145 ± 35 pg/mL for the control group, 220 ± 50 pg/mL for the type 2 diabetic group without malignant diabetic retinopathy, and 310 ± 70 pg/mL for the type 2 diabetic group with malignant diabetic retinopathy. VEGF-A showed a positive increase with glycated hemoglobin (HbA1c), duration of diabetes, and body mass index (BMI); this may infer that poor glycemic control, long-standing diabetes, and high BMI are all associated with enhanced retinal angiogenesis. Regression analysis thus showed that single nucleotide polymorphisms were an independent predictor of malignant diabetic retinopathy. Conclusions: VEGF-A represents a robust biomarker for the development of diabetic retinopathy, reflecting the activity of retinal angiogenesis independently of traditional clinical risk factors. Maintaining good blood glucose and weight control is essential for reducing vascular endothelial growth factor-A (VEGF-A) activity and slowing the progression of malignant diabetic retinopathy.

Effect of conbercept combined with dexamethasone implantation on macular thickness, visual function, retinal perfusion, and inflammatory markers in patients with diabetic macular edema: A prospective controlled study.

To evaluate the effectiveness and safety of intravitreal aflibercept 8 mg (Afl 8) for the therapy of treatment-naïve and pretreated diabetic macular edema (DME) in a clinical routine setting. A multicenter, retrospective cohort study of consecutive DME patients treated with Afl 8 over 12 months. One hundred fifty-six eyes (124 patients) with DME, including 42 (26.9%) treatment-naïve and 114 (73.1%) pretreated eyes receiving Afl 8 for 1 year. Data from electronic medical records were collected retrospectively at 5 predefined time points. The primary outcomes were the mean changes in corrected visual acuity (VA), center-point retinal thickness (CRT), central subfield thickness (CST), treatment intervals, and adverse events (AEs). Secondary outcomes included the number of injections, persistent fluid, and treatment adherence. These parameters were recorded from the beginning of anti-VEGF treatment until switching occurred in pretreated eyes. Mean change in VA, CRT, CST, treatment intervals, and AEs. In treatment-naïve eyes, VA improved from 72.9 ± 10.7 ETDRS letters at baseline to 77.7 ± 9.7 (P = 0.006); and from 73.9 ± 11.2 to 75.4 ± 10.1 ETDRS letters (P = 0.094) in pretreated eyes. Central subfield thickness decreased in both groups (naïve: 448.9 ± 154.3 μm to 320.0 ± 80.1 μm, P < 0.001; pretreated: 336.6 ± 90.5 μm to 310.2 ± 69.9 μm, P = 0.047). After 12 months, 38.1% of naïve eyes and 27.2% of pretreated eyes were free of retinal fluid in the central 1 mm. In treatment-naïve eyes, the mean treatment interval was 15.3 ± 12.0 weeks at 12 months. In pretreated eyes, the interval increased from 7.6 ± 3.7 weeks at the time of switching to 13.0 ± 9.0 weeks (P < 0.001). Two eyes (4.8%) in the naïve group and 16 eyes (14%) in the switcher group were switched away within the first year due to insufficient response to Afl 8 therapy. No AEs were reported in the treatment-naïve group. In the pretreated group, 3 cases of noninfectious intraocular inflammation (IOI; 1.9%; 1 recurrent), 2 instances of acute intraocular pressure rise, and 1 vitreous hemorrhage were reported. Afl 8 offers a promising approach to reducing the treatment burden in DME. It enables extended dosing intervals without compromising efficacy and safety, especially in refractory eyes. However, a possibly increased rate of mild IOI has been observed. Proprietary or commercial disclosure may be found in the Footnotes and Disclosures at the end of this article.

Astaxanthin protects retinal Müller cells against high glucose-induced oxidative stress through the sirtuin 1/AMPK/FOXO1 pathway.

The visual impairment in diabetic retinopathy (DR) has been associated with the pathophysiological changes of the entire visual pathway. However, only a few studies have specifically examined dynamic metabolic changes in the visual cortex of DR. The purpose of the study was to longitudinally characterize dynamic metabolic alterations in the visual cortex of DR rats using 11.7 T proton magnetic resonance spectroscopy (1H-MRS), with histopathological validation. 3-month-old male DR rats and matched healthy rats were randomly selected into the study (n = 7/group), with metabolic assessments in the visual cortex conducted at 2, 4, 6, and 8 weeks. Immunohistochemical analyses were performed at 8 weeks to evaluate visual cortex alterations. The metabolite concentration ratios were compared between DR rats and controls at different time points using repeated measures analysis of variance followed by Bonferroni post hoc tests. The comparison of immunohistochemical indicators between DR rats and controls was evaluated using independent samples t test. p < 0.05 was considered statistically significant. Compared to controls, DR rats exhibited significantly higher Ins/tCr and Cho/tCr ratios in the visual cortex at 2, 4, 6, and 8 weeks, while NAA/tCr, Glu/tCr, GABA/tCr, and Tau/tCr ratios were significantly lower, respectively (all p < 0.05). Notably, Ins/tCr and Cho/tCr progressively increased with the progression of DR, whereas NAA/tCr, Glu/tCr, GABA/tCr, and Tau/tCr gradually decreased correspondingly (all p < 0.05). At 8 weeks, DR rats showed a reduction in NeuN-, Tau-, NR2B-, and GABAA-positive cells, along with an increased expression of GFAP-positive cells, compared to controls (all p < 0.0001). In conclusion, with the progression of DR, the dynamic metabolic alterations in the visual cortex indicated ongoing cortical degeneration, impaired neurotransmitter metabolism, dysregulated cellular homeostasis and glial cell proliferation, highlighting the underlying neurobiological mechanisms of visual impairment in DR.

Ginkgolide B alleviates diabetic retinopathy by inhibiting ferroptosis in retinal vascular endothelial cells via the TSPO/Nrf2 pathway.

Resveratrol alleviated diabetic retinal neuronal ferroptosis induced by high glucose through inhibiting HIF-1α and HMOX1 pathway.

The protective effect and mechanism of phycocyanin on diabetic retinopathy in rats.

The online version contains supplementary material available at 10.1007/s13205-026-04720-3.

HVMASF++ with Zeiler and Fergus path aggregation residual deep Maxout Network for retinal vessel segmentation and multi-stage diabetic retinopathy classification

Application of diabetic retinopathy segmentation based on multi-attention and multi-scale supervision

DR-TrustNet: Enhancing diabetic retinopathy detection using reliable efficient networks and uncertainty quantification

WFDENet: Wavelet-based frequency decomposition and enhancement network for diabetic retinopathy lesion segmentation

NOP14 promotes proliferative diabetic retinopathy through ribosome biogenesis and endothelial dysfunction via Wnt/β-catenin signaling activation.

A hybrid model merging convolutional neural network and differential vision transformer for diabetic retinopathy identification

To investigate the sex-specific correlation between systemic factors and retinal neurovascular alterations in individuals with type 1 diabetes mellitus (T1DM) who do not exhibit signs of diabetic retinopathy (DR). A cohort participant without DR diagnosed with T1DM, underwent comprehensive ophthalmologic evaluation, optical coherence tomography angiography retinal structural and microvascular density analysis, and systemic parameter assessment. Multiple linear regression analysis was used to investigate the impact of systemic parameters on retinal alterations in distinct gender groups. A total of 182 individuals were included, consisting of 85 males (mean age 23.28±12.75y) and 97 females (mean age 22.98±13.68y). Males exhibited significantly greater thickness in both the internal retinal layer and the entire retina compared to females (P<0.01), whereas females had higher densities of deep retinal vessels and choroidal capillaries (P<0.05). Additionally, glycemic control was found to have a notable influence on retinal thickness in males (P<0.05), while insulin function had a more pronounced impact on retinal structure in females (P<0.01). Furthermore, a significant correlation was observed between thyroid function markers and retinal parameters in both male and female (P<0.05). Sex differences in alterations in retinal structure and microcirculation are observed in individuals with T1DM prior to the development of clinical DR, with a noted association between these changes and systemic parameters.

Growth hormone-releasing hormone (GHRH) is a hypothalamic releasing hormone that plays a crucial physiological role in regulating the synthesis and release of anterior pituitary hormones. In recent years, studies have found that GHRH possesses functions like anti-inflammation, promoting cell proliferation, and facilitating cell migration. It participates in regulating the development of uveitis and diabetic retinopathy. Additionally, it also has an impact on the development of retinal ganglion cells by modulating the inflammatory response and mediating the immune response. Given the important roles of GHRH in ophthalmic diseases, elucidating the molecular regulation of the GHRH-GHRH receptor (GHRHR) signal and the innovative development of intervention pathways that directly or indirectly target GHRH serve as strong evidence of how basic research guides innovation and translation. In this review, research reports on GHRH in ophthalmic diseases including retinal diseases and uveitis were summarized and analyzed.