Abstract: Retinal degeneration, a leading cause of irreversible blindness, often results from photoreceptor deterioration due to genetic mutations or damage to retinal pigment epithelial (RPE) cells. Emerging research highlights the gut-eye axis, a connection between gut microbiota and eye diseases. Our recent findings demonstrate that bacterial translocation from the gut to the retina contributes to Crb1-associated retinal degeneration. This review explores the relationship between the gut microbiome and retinal degeneration, focusing on inherited retinal degeneration (IRD) and age-related macular degeneration (AMD).

Abstract: Retinal degeneration, a leading cause of irreversible blindness, often results from photoreceptor deterioration due to genetic mutations or damage to retinal pigment epithelial (RPE) cells. Emerging research highlights the gut-eye axis, a connection between gut microbiota and eye diseases. Our recent findings demonstrate that bacterial translocation from the gut to the retina contributes to Crb1-associated retinal degeneration. This review explores the relationship between the gut microbiome and retinal degeneration, focusing on inherited retinal degeneration (IRD) and age-related macular degeneration (AMD).

Amblyopia is a neurodevelopmental vision disorder resulting from abnormal visual input during the critical period of visual development, such as strabismus, uncorrected anisometropia, high refractive errors, and form deprivation. It is frequently associated with reduced visual acuity and deficits in binocular vision. Traditional occlusion therapy for amblyopia has typically been restricted to infants and young children during the critical period of visual development, as it is believed to be ineffective for older children and adults due to the decreased plasticity of the mature brain. Our research group has concentrated on pivotal scientific issues in amblyopia, including quantitative methods for detecting binocular vision, especially interocular visual suppression, the mechanisms underlying binocular vision impairment in amblyopia,treatment methods and their evaluations for amblyopia, and visual plasticity and its neural mechanismsin amblyopia. This paper summarizes the visual mechanisms and treatment modalities of amblyopia based on our research and both domestic and foreign sources, while also looking forward to the future development of this field in light of existing problems.

Amblyopia is a neurodevelopmental vision disorder resulting from abnormal visual input during the critical period of visual development, such as strabismus, uncorrected anisometropia, high refractive errors, and form deprivation. It is frequently associated with reduced visual acuity and deficits in binocular vision. Traditional occlusion therapy for amblyopia has typically been restricted to infants and young children during the critical period of visual development, as it is believed to be ineffective for older children and adults due to the decreased plasticity of the mature brain. Our research group has concentrated on pivotal scientific issues in amblyopia, including quantitative methods for detecting binocular vision, especially interocular visual suppression, the mechanisms underlying binocular vision impairment in amblyopia,treatment methods and their evaluations for amblyopia, and visual plasticity and its neural mechanismsin amblyopia. This paper summarizes the visual mechanisms and treatment modalities of amblyopia based on our research and both domestic and foreign sources, while also looking forward to the future development of this field in light of existing problems.

Aims: To identify the characteristic retinal neurovascular changes in patients in different stages of nondiabetic chronic kidney disease (CKD) and to develop a model for the accurate diagnosis of nondiabetic CKD.
Methods: Peripapillary retinal nerve fiber layer (pRNFL) thickness and average macular ganglion cell-inner plexiform layer (GC-IPL) thickness of nondiabetic CKD patients and healthy controls (HC) were evaluated by spectral-domain optical coherence tomography (OCT). The vessel density (VD) and perfusion density (PD) of the macula were obtained from optical coherence tomography angiography (OCTA). The estimated glomerular filtration rate (eGFR) was obtained to access the kidney function of CKD patients. Multiple linear regression models were used to adjust for confounding factors in statistical analyzes. The diagnostic capabilities of the parameters were evaluated by logistic regression models.
Results: 131 nondiabetic CKD patients and 62 HC entered the study. eGFR was found significantly associated with parafoveal VD and PD (average PD: β = 0.000 4, P_adjusted < 0.001) in various sectors. Thinning of pRNFL (β = -6.725, P_adjusted < 0.001) and GC-IPL (β = -4.542, P_adjusted < 0.001), as well as decreased VD (β = -2.107, P_- adjusted < 0.001) and PD (β = -0.057, P_adjusted = 0.032 8) were found in CKD patients. Thinning of pRNFL and deteriorated perifoveal vasculature were found in early CKD, and the parafoveal and foveal VD significantly declined in advanced CKD. Logistic regression models were employed, and selected neurovascular parameters showed an AUC of 0.853 (95% Confidence Interval [CI]: 0.795 to 0.910) in distinguishing CKD patients from HC.
Conclusions: Distinctive retinal neurovascular characteristics could be observed in nondiabetic CKD patients of different severities. Our results suggest that retinal manifestations could be valuable in the screening, diagnosis, and follow-up evaluation of patients with CKD.

Aims: To identify the characteristic retinal neurovascular changes in patients in different stages of nondiabetic chronic kidney disease (CKD) and to develop a model for the accurate diagnosis of nondiabetic CKD.
Methods: Peripapillary retinal nerve fiber layer (pRNFL) thickness and average macular ganglion cell-inner plexiform layer (GC-IPL) thickness of nondiabetic CKD patients and healthy controls (HC) were evaluated by spectral-domain optical coherence tomography (OCT). The vessel density (VD) and perfusion density (PD) of the macula were obtained from optical coherence tomography angiography (OCTA). The estimated glomerular filtration rate (eGFR) was obtained to access the kidney function of CKD patients. Multiple linear regression models were used to adjust for confounding factors in statistical analyzes. The diagnostic capabilities of the parameters were evaluated by logistic regression models.
Results: 131 nondiabetic CKD patients and 62 HC entered the study. eGFR was found significantly associated with parafoveal VD and PD (average PD: β = 0.000 4, P_adjusted < 0.001) in various sectors. Thinning of pRNFL (β = -6.725, P_adjusted < 0.001) and GC-IPL (β = -4.542, P_adjusted < 0.001), as well as decreased VD (β = -2.107, P_adjusted < 0.001) and PD (β = -0.057, P_adjusted = 0.032 8) were found in CKD patients. Thinning of pRNFL and deteriorated perifoveal vasculature were found in early CKD, and the parafoveal and foveal VD significantly declined in advanced CKD. Logistic regression models were employed, and selected neurovascular parameters showed an AUC of 0.853 (95% Confidence Interval [CI]: 0.795 to 0.910) in distinguishing CKD patients from HC.
Conclusions: Distinctive retinal neurovascular characteristics could be observed in nondiabetic CKD patients of different severities. Our results suggest that retinal manifestations could be valuable in the screening, diagnosis, and follow-up evaluation of patients with CKD.

Aims: To explore the point-wise correlations between 10-2 visual field (VF) metrics and macular vessel density, as measured by optical coherence tomography angiography (OCTA), in patients with early open-angle glaucoma (OAG) and healthy controls. Methods: This is a cross-sectional study that retrospectively analyzed data from 54 participants (18 eraly OAG patients and 36 healthy controls) from the Zhongshan Ophthalmic Center. All participants underwent comprehensive ophthalmic examinations, 10-2 VF, and macular OCTA imaging. The correlation between capillary density (CD) in macular subregions and light sensitivity (LS) at corresponding VF test points was analyzed using Pearson's correlation coefficients. Results: The analysis revealed a significant reduction in CD within the inferior macular regions of glaucomatous eyes. Notably, there were strong point-wise correlations between CD and 10-2 VF, particularly in the inferior region of outer ring (peak r = 0.534, P < 0.001). Conclusion: The point-wise correlation between 10-2 VF and macular CDdemonstrates the potential for using CD to predict central VF damage in glaucoma, emphasizing theimportance of macular microcirculation in early disease screening.

Aims: To explore the point-wise correlations between 10-2 visual field (VF) metrics and macular vessel density, as measured by optical coherence tomography angiography (OCTA), in patients with early open-angle glaucoma (OAG) and healthy controls. Methods: This is a cross-sectional study that retrospectively analyzed data from 54 participants (18 early OAG patients and 36 healthy controls) from the Zhongshan Ophthalmic Center. All participants underwent comprehensive ophthalmic examinations, 10-2 VF, and macular OCTA imaging. The correlation between capillary density (CD) in macular subregions and light sensitivity (LS) at corresponding VF test points was analyzed using Pearson's correlation coefficients. Results: The analysis revealed a significant reduction in CD within the inferior macular regions of glaucomatous eyes. Notably, there were strong point-wise correlations between CD and 10-2 VF, particularly in the inferior region of outer ring (peak r = 0.534, P < 0.001). Conclusion: The point-wise correlation between 10-2 VF and macular CDdemonstrates the potential for using CD to predict central VF damage in glaucoma, emphasizing theimportance of macular microcirculation in early disease screening.

Aims: This study describes vascular abnormalities in X-linked retinoschisis (XLRS) using fundus fluorescein angiography (FFA) and ultra-widefield swept-source optical coherence tomography angiography (UWF SS-OCTA) to better understand the disease's vascular features and impact. Methods: A retrospective cross-sectional study was conducted on 26 XLRS patients (46 eyes). A comprehensive ophthalmic examination was performed, including FFA and UWF SS-OCTA. FFA abnormalities were divided into peripheral schisis-associated and optic disc-associated types. Results: The mean age of patients was 11.3±6.5 years. Macular schisis appeared in 97.8% of eyes, peripheral schisis in 89.1%, and peripheral bullous schisis (PBS) in 67.39%. Major vascular changes identified by FFA included dendritic capillary dilation/leakage (91.3%), internal residual vessel leakage (78.3%), and capillary dropout/ischemia (71.7%). Minor changes included zonal retinal pigment epithelium (RPE) proliferation (6.5%), bridging vessels (4.4%), and capillary sheathing (4.4%). peripapillary choroidal neovascularization (PPCNV) was noted in 10.9% and situs inversus of optic disc in 13.0% of eyes. Additionally, situs inversusof optic disc and zonal RPE proliferation were novel findings. Major FFA changes correlated with broader PBS (P = 0.045) (P ＜ 0.001) (P = 0.003). Clock hours of PBS were significant predictors for internal residual vessel leakage (OR = 0.30, P = 0.03). No significant correlation was found between gene mutation type and FFA abnormalities(P = 1.000)(P = 0.539). Conclusions: This study highlighted the significant prevalence (95.7%) of vascular abnormalities in XLRS and emphasized the importance of combining FFA with UWF SS-OCTA for comprehensive evaluation, enhancing the understanding of XLRS pathophysiology and aiding in targeted treatment approaches.

Aims: This study describes vascular abnormalities in X-linked retinoschisis (XLRS) using fundus fluorescein angiography (FFA) and ultra-widefield swept-source optical coherence tomography angiography (UWF SS-OCTA) to better understand the disease's vascular features and impact. Methods: A retrospective cross-sectional study was conducted on 26 XLRS patients (46 eyes). A comprehensive ophthalmic examination was performed, including FFA and UWF SS-OCTA. FFA abnormalities were divided into peripheral schisis-associated and optic disc-associated types. Results: The mean age of patients was 11.3±6.5 years. Macular schisis appeared in 97.8% of eyes, peripheral schisis in 89.1%, and peripheral bullous schisis (PBS) in 67.39%. Major vascular changes identified by FFA included dendritic capillary dilation/leakage (91.3%), internal residual vessel leakage (78.3%), and capillary dropout/ischemia (71.7%). Minor changes included zonal retinal pigment epithelium (RPE) proliferation (6.5%), bridging vessels (4.4%), and capillary sheathing (4.4%). peripapillary choroidal neovascularization (PPCNV) was noted in 10.9% and situs inversus of optic disc in 13.0% of eyes. Additionally, situs inversusof optic disc and zonal RPE proliferation were novel findings. Major FFA changes correlated with broader PBS (P = 0.045) (P ＜ 0.001) (P = 0.003). Clock hours of PBS were significant predictors for internal residual vessel leakage (OR = 0.30, P = 0.03). No significant correlation was found between gene mutation type and FFA abnormalities(P = 0.539). Conclusions: This study highlighted the significant prevalence (95.7%) of vascular abnormalities in XLRS and emphasized the importance of combining FFA with UWF SS-OCTA for comprehensive evaluation, enhancing the understanding of XLRS pathophysiology and aiding in targeted treatment approaches.

Age stands as a primary risk factor for diseases and disabilities among the elderly. To effectively assess the underlying aging processes, accurate measures of biological age and rates of aging across multiple levels of aging features are essential. Biological age derives from physiological assessments of systems and organs. It has emerged as a superior predictor of age-related diseases and mortality compared to chronological age. Recent advancements in machine learning have catalyzed the development of sophisticated models capable of quantitatively characterizing biological aging with different types of data. This review explores the machine learning models in advancing our understanding of biological aging, highlighting the potential of these innovative approaches to facilitate aging research and personalized healthcare strategies.

Age stands as a primary risk factor for diseases and disabilities among the elderly. To effectively assess the underlying aging processes, accurate measures of biological age and rates of aging across multiple levels of aging features are essential. Biological age derives from physiological assessments of systems and organs. It has emerged as a superior predictor of age-related diseases and mortality compared to chronological age. Recent advancements in machine learning have catalyzed the development of sophisticated models capable of quantitatively characterizing biological aging with different types of data. This review explores the machine learning models in advancing our understanding of biological aging, highlighting the potential of these innovative approaches to facilitate aging research and personalized healthcare strategies.

Purpose: To identify plasma proteins that are causally related to primary open-angle glaucoma (POAG) for potential therapeutic targeting. Methods: Summary statistics of plasma protein quantitative trait loci (pQTL) were derived from two extensive genome-wide analysis study (GWAS) datasets and one systematic review, with over 100 thousand participants covering thousands of plasma proteins. POAG data were sourced from the largest FinnGen study, comprising 8,530 DR cases and 391,275 European controls. A two-sample MR analysis, supplemented by bidirectional MR, Bayesian co-localization analysis, and phenotype scanning, was conducted to examine the causal relationships between plasma proteins and POAG. The analysis was validated by identifying associations between plasma proteins and POAG-related traits, including intraocular pressure (IOP), retinal nerve fibre layer (RNFL), and ganglion cell and inner plexiform layer (GCIPL). By searching druggable gene lists, the ChEMBL database, and the ClinicalTrials.gov database, the druggability and clinical development activity of the identified proteins were systematically evaluated. Results: Eighteen proteins were identified with significant associations with POAG risk after multiple comparison adjustments. The ORs per standard deviation increase in protein levels ranged from 0.39 (95% CI: 0.24–0.62; P = 7.70×10-5) for phospholipase C gamma 1 (PLCG1) to 1.29 (95% CI: 1.16–1.44; P = 6.72×10-6) for nidogen-1 (NID1). Bidirectional MR indicated that reverse causality did not interfere with the results of the main MR analyses. Five proteins exhibited strong co-localization evidence (PH4 ≥ 0.8): protein sel-1 homolog 1 (SEL1L), tyrosine-protein kinase receptor UFO (AXL), nidogen-1 (NID1) and FAD-linked sulfhydryl oxidase ALR (GFER) were negatively associated with POAG risk, while roundabout homolog 1 (ROBO1) showed a positive association. The phenotype scanning did not reveal any confounding factors between pQTLs and POAG. Further, validation analyses identified nine proteins causally related to POAG traits, with five proteins including interleukin-18 receptor 1 (IL18R1), interleukin-1 receptor type 1 (IL1R1), phospholipase C gamma 1 (PLCG1), ribonuclease pancreatic (RNASE1), serine protease inhibitor Kazal-type 6 (SPINK6) revealing consistent directional associations. In addition, 18 causal proteins were highlighted for their druggability, of which 5 proteins are either already approved drugs or in clinical trials and 13 proteins are novel drug targets. Conclusions: This study identifies 18 plasma proteins as potential therapeutic targets for POAG, particularly emphasizing the role of genomic and proteomic integration in drug discovery. Future experimental and clinical studies should be conducted to validate the efficacy of these proteins and to conduct more comprehensive proteomic explorations, thus taking a significant leap toward innovative POAG treatments.

Purpose: To identify plasma proteins that are causally related to primary open-angle glaucoma (POAG) for potential therapeutic targeting. Methods: Summary statistics of plasma protein quantitative trait loci (pQTL) were derived from two extensive genome-wide analysis study (GWAS) datasets and one systematic review, with over 100 thousand participants covering thousands of plasma proteins. POAG data were sourced from the largest FinnGen study, comprising 8,530 DR cases and 391,275 European controls. A two-sample MR analysis, supplemented by bidirectional MR, Bayesian co-localization analysis, and phenotype scanning, was conducted to examine the causal relationships between plasma proteins and POAG. The analysis was validated by identifying associations between plasma proteins and POAG-related traits, including intraocular pressure (IOP), retinal nerve fibre layer (RNFL), and ganglion cell and inner plexiform layer (GCIPL). By searching druggable gene lists, the ChEMBL database, and the ClinicalTrials.gov database, the druggability and clinical development activity of the identified proteins were systematically evaluated. Results: Eighteen proteins were identified with significant associations with POAG risk after multiple comparison adjustments. The ORs per standard deviation increase in protein levels ranged from 0.39 (95% CI: 0.24–0.62; P = 7.70×10-5) for phospholipase C gamma 1 (PLCG1) to 1.29 (95% CI: 1.16–1.44; P = 6.72×10-6) for nidogen-1 (NID1). Bidirectional MR indicated that reverse causality did not interfere with the results of the main MR analyses. Five proteins exhibited strong co-localization evidence (PH4 ≥ 0.8): protein sel-1 homolog 1 (SEL1L), tyrosine-protein kinase receptor UFO (AXL), nidogen-1 (NID1) and FAD-linked sulfhydryl oxidase ALR (GFER) were negatively associated with POAG risk, while roundabout homolog 1 (ROBO1) showed a positive association. The phenotype scanning did not reveal any confounding factors between pQTLs and POAG. Further, validation analyses identified nine proteins causally related to POAG traits, with five proteins including interleukin-18 receptor 1 (IL18R1), interleukin-1 receptor type 1 (IL1R1), phospholipase C gamma 1 (PLCG1), ribonuclease pancreatic (RNASE1), serine protease inhibitor Kazal-type 6 (SPINK6) revealing consistent directional associations. In addition, 18 causal proteins were highlighted for their druggability, of which 5 proteins are either already approved drugs or in clinical trials and 13 proteins are novel drug targets. Conclusions: This study identifies 18 plasma proteins as potential therapeutic targets for POAG, particularly emphasizing the role of genomic and proteomic integration in drug discovery. Future experimental and clinical studies should be conducted to validate the efficacy of these proteins and to conduct more comprehensive proteomic explorations, thus taking a significant leap toward innovative POAG treatments.

Objective: To investigate the lifestyle and myopia among primary school students in urban areas of Fujian with the context of myopia prevention and control measures, aiming to provide scientific evidence for identifying high-risk myopia population and formulating effective intervention strategies. 

Methods: A cross-sectional study was conducted from October to November 2023, enrolling 811 fourth-grade students from three primary schools in three cities across Fujian. Personal information and lifestyle-related pattern were collected using customized questionnaire. Participants underwent comprehensive ophthalmic assessments including distance visual acuity tests and refractive examinations. Logistic regression analysis was used to assess the impact of lifestyle on the onset of myopia.

Results: The prevalence of myopia among fourth-grade students in urban primary schools in Fujian was 46.4%. Only 25.8% students engaged in outdoor activities for more than 2 hours daily, while63.3% participated in outdoor activities during class breaks. Multivariate Logistic regression analysis revealed that outdoor activities during class breaks (OR= 0.646 [95% confidence interval(CI): 0.473-0.881], P = 0.006) and daily time spent outdoors (2-3 hours, OR=0.682 [95%CI：0.466-0.993], P=0.047; more than 3 hours, OR=0.403 [95%CI: 0.192-0.796], P = 0.01) were independent protective factors against myopia. Lifestyle significantly enhanced the predictive performance for myopia (P = 0.01). Additionally, parental myopia (one parent with myopia, OR=2.247 [95%CI: 1.612- 3.145], P < 0.001; both parents with myopia, OR=4.824 [95%CI: 3.262-7.204], P < 0.001) emerged as a key risk factor for myopia.

Conclusion: There is considerable scope for improving the lifestyle of primary school students in urban areas of Fujian. Lifestyle is strongly associated with myopia onset, highlighting the need for schools and families to actively encourage students to engage in more outdoor activities and take breaks outdoors to prevent and control myopia. Students with parents, especially both parents, having myopia should be considered as a key target group for myopia prevention efforts.

Objective: To investigate the lifestyle and myopia among primary school students in urban areas of Fujian with the context of myopia prevention and control measures, aiming to provide scientific evidence for identifying high-risk myopia population and formulating effective intervention strategies. 

Methods: A cross-sectional study was conducted from October to November 2023, enrolling 811 fourth-grade students from three primary schools in three cities across Fujian. Personal information and lifestyle-related pattern were collected using customized questionnaire. Participants underwent comprehensive ophthalmic assessments including distance visual acuity tests and refractive examinations. Logistic regression analysis was used to assess the impact of lifestyle on the onset of myopia.

Results: The prevalence of myopia among fourth-grade students in urban primary schools in Fujian was 46.4%. Only 25.8% students engaged in outdoor activities for more than 2 hours daily, while63.3% participated in outdoor activities during class breaks. Multivariate Logistic regression analysis revealed that outdoor activities during class breaks (OR= 0.646 [95% confidence interval(CI): 0.473-0.881], P = 0.006) and daily time spent outdoors (2-3 hours, OR=0.682 [95%CI：0.466-0.993], P=0.047; more than 3 hours, OR=0.403 [95%CI: 0.192-0.796], P = 0.01) were independent protective factors against myopia. Lifestyle significantly enhanced the predictive performance for myopia (P = 0.01). Additionally, parental myopia (one parent with myopia, OR=2.247 [95%CI: 1.612- 3.145], P < 0.001; both parents with myopia, OR=4.824 [95%CI: 3.262-7.204], P < 0.001) emerged as a key risk factor for myopia.

Conclusion: There is considerable scope for improving the lifestyle of primary school students in urban areas of Fujian. Lifestyle is strongly associated with myopia onset, highlighting the need for schools and families to actively encourage students to engage in more outdoor activities and take breaks outdoors to prevent and control myopia. Students with parents, especially both parents, having myopia should be considered as a key target group for myopia prevention efforts.

The congenital cataract is one of the leading causes of treatable childhood blindness. Existing classification systems for congenital cataracts are primarily utilized for the diagnosis of the disease. However, these systems provide limited information necessary for the evaluation, formulation, and optimization of treatment plans. Furthermore, research on the classification of congenital cataracts still requires exploration to provide additional evidence supporting molecular diagnosis and syndromic disease diagnosis. This paper reviews relevant studies on the classification of congenital cataracts and discusses the prospects for future research in this area.

The congenital cataract is one of the leading causes of treatable childhood blindness. Existing classification systems for congenital cataracts are primarily utilized for the diagnosis of the disease. However, these systems provide limited information necessary for the evaluation, formulation, and optimization of treatment plans. Furthermore, research on the classification of congenital cataracts still requires exploration to provide additional evidence supporting molecular diagnosis and syndromic disease diagnosis. This paper reviews relevant studies on the classification of congenital cataracts and discusses the prospects for future research in this area.

Meibomian gland dysfunction (MGD) manifests through two main clinical presentations, characterized by the meibomian gland (MG) ductal obstruction or acinar dropout. While previous research has predominantly associated MGD pathogenesis with hyperkeratinization-related MG ductal obstruction and subsequent acinar atrophy, recent cases have shown significant functional acinar loss in the absence of apparent ductal keratinization or blockage. The deterioration of either MG obstruction or dropout exacerbates the condition of the other, suggesting an independent yet interconnected relationship that perpetuates the vicious cycle of MGD. Understanding the distinct pathological features of MG obstruction and dropout is crucial for delineating their etiology and identifying targeted therapeutic strategies. This review explores the nuanced interrelations of MG obstruction and dropout, elucidating potential pathological mechanisms to establish a foundation for early MGD diagnosis and intervention.

Meibomian gland dysfunction (MGD) manifests through two main clinical presentations, characterized by the meibomian gland (MG) ductal obstruction or acinar dropout. While previous research has predominantly associated MGD pathogenesis with hyperkeratinization-related MG ductal obstruction and subsequent acinar atrophy, recent cases have shown significant functional acinar loss in the absence of apparent ductal keratinization or blockage. The deterioration of either MG obstruction or dropout exacerbates the condition of the other, suggesting an independent yet interconnected relationship that perpetuates the vicious cycle of MGD. Understanding the distinct pathological features of MG obstruction and dropout is crucial for delineating their etiology and identifying targeted therapeutic strategies. This review explores the nuanced interrelations of MG obstruction and dropout, elucidating potential pathological mechanisms to establish a foundation for early MGD diagnosis and intervention.