Purpose:Retinitis pigmentosa (RP) is a hereditary retinal disorder distinguished by progressive photoreceptor cell (PRC) loss, in which glial activation can accelerate degeneration. Diosgenin, a natural steroidal sapogenin with potent anti-inflammatory properties, has shown therapeutic potential for ocular and neurodegenerative diseases but has not been explored for retinal degeneration. This study examined the protective role of diosgenin against PRC degeneration and explored potential anti-inflammatory mechanisms in an N-methyl-N-nitrosourea (MNU)-induced mouse model of retinal degeneration. Methods:The model was established by intraperitoneal injection of 50 mg/kg MNU, followed by oral gavage of diosgenin/lutein (positive control)/vehicle. The effects of diosgenin on PRC structure, apoptosis, retinal function, and glial activation were evaluated. Network pharmacology and molecular docking were used to investigate potential mechanisms. Results:Diosgenin preserved retinal integrity and function in MNU-induced mice, with relative preservation of the outer nuclear layer thickness and outer segment (OS) length of rods and cones. Disorganization of OS membrane discs and abnormal morphology of organelles were attenuated, while fundus photographs showed fewer lesions. Furthermore, diosgenin mitigated PRC apoptosis and maintained retinal light responses. Mechanistically, diosgenin ameliorated reactive gliosis of Müller glial cells (MGCs), attenuated the expression levels of inflammatory cytokines and chemokines, and mitigated activation of the IL6ST/JAK2/STAT3 pathway. Conclusions:Diosgenin attenuated PRC degeneration in MNU-induced mice, and one of its mechanisms may involve the attenuation of reactive gliosis in MGCs and inflammatory responses, with possible involvement of the IL6ST/JAK2/STAT3 pathway. Diosgenin may serve as a potential intervention candidate for retinal degenerative diseases, such as RP.

The cytoplasmic dynein complex mediates retrograde transport of various intracellular components and plays a critical role in mitosis, nuclear migration, organelle positioning, vesicle trafficking, misfolded protein clearance, and intercellular signaling. Mutations in human cytoplasmic dynein subunits and regulators have been directly linked to various neurological diseases and are increasingly recognized as contributors to ocular degenerative diseases. However, the precise mechanisms underlying ocular morphogenesis and degeneration remain poorly understood. Various animal models, including Drosophila, mouse, and zebrafish, have been established to investigate the pathogenesis of cytoplasmic dynein complex-related ocular disorders. Findings from these models indicate that dynein complex-related ocular pathologies often involve endoplasmic reticulum stress, impaired Notch signaling, and disrupted Sonic Hedgehog pathways. Systematically integrating gene functional data and molecular mechanism clues derived from different models can help refine the “gene-phenotype-mechanism” correlation network and may ultimately advance precision diagnosis and targeted therapy. Emerging evidence has highlighted the cytoplasmic dynein complex as a key factor in ocular development and disease. Integrating findings across model systems may enable more precise diagnosis and the development of targeted interventions for dynein-related ocular disorders.

Diabetic retinopathy (DR) is a leading cause of blindness among adults worldwide, with hyperglycemia-induced oxidative stress lies at the core of its pathogenesis. This review synthesises evidence showing that elevated glucose, hypoxia and pro-inflammatory mediators act synergistically to impair the mitochondrial electron-transport chain and activate NADPH oxidase, thereby generating excess reactive oxygen species (ROS). These ROS, in turn, potentiate the polyol, protein kinase C, hexosamine and advanced-glycation end-product pathways, creating a metabolic-memory-driven vicious circle that disrupts the blood-retina barrier, promotes capillary closure and triggers neurodegenerative damage. We further delineate the ROS-dependent molecular networks underlying endoplasmic-reticulum stress, inflammation and apoptosis, and summarize preclinical and early clinical data on the efficacy of antioxidant therapies. By integrating the latest mechanistic insights with emerging intervention strategies, we propose that multi-target approaches directed at oxidative stress may attenuate DR progression and offer a rational framework for developing safe and effective retinal-protective treatments. METHODS:We undertook a narrative review and conducted searches of the PubMed and Web of Science databases from inception to June 25, 2025, restricting results to English-language publications. The search keywords were: diabetic retinopathy, oxidative stress, reactive oxygen species, mitochondria, NADPH oxidase, endoplasmic reticulum stress, unfolded protein response, ferroptosis, and antioxidants. INCLUSION CRITERIA:reports were eligible if they focused on diabetic retinopathy and addressed at least one of the following: oxidative stress or ROS biology; mitochondrial dysfunction; NADPH oxidase; ER stress/UPR; ferroptosis; gut-retina axis with oxidative-stress relevance; AI/ML-derived oxidative-stress or ferroptosis signatures for DR stratification; or antioxidant/ROS-targeting interventions in cellular, animal, or human studies. Both original studies (in vitro, in vivo, clinical, and trials) and reviews used for contextualization were considered. EXCLUSION CRITERIA:we excluded non-DR ocular conditions without a clearly stated link to DR oxidative/ER-stress mechanisms; articles not in English; conference abstracts without full reports; preprints without peer review; case reports lacking mechanistic or outcome data; and opinion pieces or editorials unless they provided population-health context directly relevant to DR. Titles/abstracts and then full texts were screened independently by two authors with disagreements resolved by discussion and, when needed, consultation with a third reviewer. In keeping with the narrative nature of this review, we did not conduct a formal tool-based risk-of-bias assessment. Instead, included studies were qualitatively appraised for topical relevance to oxidative- and ER-stress mechanisms in DR, appropriateness of models and methods, and clarity of outcomes.

Purpose:Retinitis pigmentosa (RP) is a hereditary retinal disease characterized by progressive photoreceptor cell (PRC) degeneration. WD repeat domain 34 (WDR34), an intermediate chain of dynein-2, is essential for retrograde intraflagellar transport (IFT). However, the mechanisms by which WDR34 deficiency causes retinal degeneration remain unclear. This study aims to investigate the impact of WDR34 deficiency on retrograde IFT and its contribution to retinal degeneration. Methods:WDR34 deficiency was modeled in vivo via subretinal injection of adeno-associated virus-shRNA-WDR34 and in vitro by CRISPR/Cas9-mediated knockout in 661W cells. Retinal degeneration and IFT defects were assessed by histologic, functional, and ultrastructural analyses. Proteomic analysis followed by in vivo validation was used to investigate the molecular mechanism underlying WDR34-deficient retinal degeneration. Results:WDR34 knockdown induced progressive retinal degeneration characterized by PRC apoptosis, gradual outer nuclear layer thinning, reduced electroretinography responses, and outer segment shortening. WDR34 deficiency impaired retrograde IFT and caused rhodopsin and opsin mislocalization. These alterations induced endoplasmic reticulum stress and unfolded protein response (UPR) activation, activating the IRE1α/TRAF2/NF-κB signaling pathway, ultimately contributing to retinal inflammation and degeneration. Conclusions:WDR34 is crucial for maintaining retrograde IFT in PRCs. WDR34 deficiency disrupts outer segment maintenance and triggers UPR-mediated inflammatory responses and apoptosis, ultimately leading to retinal degeneration. This study reveals a novel mechanistic link among WDR34, retrograde IFT, ciliopathies, and retinal degeneration, providing potential therapeutic insights for ciliopathy-associated RP.

PURPOSE. Retinitis pigmentosa (RP) is a hereditary retinal disease characterized by progressive degeneration of photoreceptor cells (PRCs). Identifying potential pathogenic genes and understanding the mechanisms of PRC degeneration are essential for improving diagnosis and treatment. Cytoplasmic dynein 1, responsible for retrograde axonal transport along microtubules, plays critical roles in neuronal function. This study utilized dync1h1-deficient zebrafish to investigate its roles in PRC morphogenesis and degeneration. METHODS. Heterozygous and homozygous dync1h1-deficient zebrafish were confirmed through Sanger sequencing. Morphological changes and retinal phenotypes were assessed through histological analysis. RNA sequencing and bioinformatics were used to explore molecular mechanisms in dync1h1-/- zebrafish, with endoplasmic reticulum (ER) stress and apoptosis pathways validated in vivo. RESULTS. Dync1h1-/- zebrafish exhibit severe developmental defects, including microphthalmia, disorganized retinal lamination, and PRC apoptosis. In dync1h1+/-, mild but progressive growth retardation and PRC defects were observed. Dync1h1 loss impaired retrograde axonal transport, leading to defects in cilium biogenesis and transport disorder of phototransduction proteins in PRCs. This triggered ER stress, activating BiP-ATF4CHOP signaling pathway and leading to PRC degeneration. CONCLUSIONS. Dync1h1 is essential for maintaining retrograde axonal transport and proper trafficking of phototransduction proteins in PRCs. Non-resolving ER stress-induced PRC apoptosis is a key factor in DYNC1H1-associated retinal degeneration. This study provides important insights into the precise diagnosis and may help in the development of targeted therapies for retinal degenerative diseases.

Pars plana vitrectomy is the standard treatment for several vitreoretinal diseases. Continuous improvements in ophthalmic surgical techniques have led to excellent postoperative recovery of the anatomic structure of the fundus. However, postoperative visual outcomes are not always satisfactory. A literature search of articles published before 31 December 2022 was conducted on PubMed using the following keywords: “diabetic retinopathy,” “rhegmatogenous retinal detachment,” “idiopathic epiretinal membrane,” “idiopathic macular hole,” “vitrectomy,” “optical coherence tomography,” “optical coherence tomography angiography,” “microstructure,” “microstructural,” “hemodynamic,” “hemodynamics,” and “microcirculation.” Additional studies were identified by hand-searching references for relevant studies. Articles were screened for language, repetition, and relevance to the direction of study. Studies with a sample size ≥ 7 and the final follow-up time ≥ 4 weeks after vitrectomy were included in this review. Only articles published in English were included. Articles not related to our topic were excluded. Reviews and single case reports were excluded. We structured this review by disease category. The thickness of the retina and choroid, the area of the foveal avascular zone, the vessel density of the retinal and choroidal capillary plexus, and the potential association of related parameters with postoperative visual outcomes are the main outcome measures of studies included in this review. A total of 48 studies were included in this review. There were contradictory results regarding the association between postoperative microcirculatory parameters and visual acuity in patients with diabetic macular edema, with some studies concluding that improvement in perimacular microcirculation may be an important factor that affects visual acuity, and others concluded that postoperative improvement in visual acuity was not related to changes in macular blood flow. The results of studies on the relationship between postoperative microstructural and microcirculatory parameters and visual acuity in rhegmatogenous retinal detachment, idiopathic epiretinal membrane, and idiopathic macular hole eyes have been inconsistent. In gas tamponade macula-off rhegmatogenous retinal detachment eyes, postoperative best-corrected visual acuity has been reported to correlate positively with vessel density of deep capillary plexus and negatively with foveal avascular zone area of superficial capillary plexus and deep capillary plexus. In silicone oil tamponade macula-off rhegmatogenous retinal detachment eyes, best-corrected visual acuity has been reported to be positively correlated with the retinal thickness of the parafoveal 3 mm temporal quadrant and positively correlated with the vessel density of the superficial capillary plexus in the foveal, parafoveal, and perifoveal area. In addition, best-corrected visual acuity was worse and associated with reduced thickness of the inner retina, ganglion cell layer, outer plexiform layer, and outer nuclear layer in silicone oil tamponade rhegmatogenous retinal detachment eyes compared to gas tamponade. Postoperative best-corrected visual acuity in idiopathic epiretinal membrane eyes was positively correlated with the foveal avascular zone area but negatively correlated with full retinal thickness and inner retinal thickness in the foveal and parafoveal areas. Improvement in postoperative best-corrected visual acuity in idiopathic macular hole eyes was associated with reduced inner retinal thickness and reduced foveal avascular zone area. Microstructural and hemodynamic changes are involved in the recovery process after PPV for different vitreoretinal diseases. The thickness of each retinal layer in different regions of the macula, foveal avascular zone area, and vessel density of different retinal capillary plexuses in different macular regions may be potential prognostic factors for postoperative visual recovery. However, the results of the existing literature are inconsistent and require further study.

The Crumbs protein (CRB) family plays a crucial role in maintaining the apical-basal polarity and integrity of embryonic epithelia. The family comprises different isoforms in different animals and possesses diverse structural, localization, and functional characteristics. Mutations in the human CRB1 or CRB2 gene may lead to a broad spectrum of retinal dystrophies. Various CRB-associated experimental models have recently provided mechanistic insights into human CRB-associated retinopathies. The knowledge obtained from these models corroborates the importance of CRB in retinal development and maintenance. Therefore, complete elucidation of these models can provide excellent therapeutic prospects for human CRB-associated retinopathies. In this review, we summarize the current animal models and human-derived models of different CRB family members and describe the main characteristics of their retinal phenotypes.

BACKGROUND:Presently, the global prevalence of myopia and high myopia reaches approximately 1.95 billion and 277 million individuals, respectively. Projections suggest that by 2050, the number of people with myopia may rise to 4.758 billion and those with high myopia to 938 million. In highly myopic eyes, the occurrence of MF is reported to be as high as 8-33%. SUMMARY:This review comprehensively addresses the classification, pathogenesis, natural progression, concomitant pathologies, and therapeutic strategies for macular foveoschisis in highly myopic patients. KEY MESSAGES:In recent years, macular foveoschisis has emerged as a prevalent complication in individuals with high myopia, primarily resulting from the combination of inward traction by vitreoretinal adhesions and outward traction exerted by posterior scleral staphyloma on the retina. While some maintain partial visual stability over an extended period, others may progress to macular holes or even retinal detachment. For highly myopic patients with macular foveoschisis, the mainstay procedures are vitrectomy, macular buckle, and posterior scleral reinforcement. However, there is controversy about whether to perform inner limiting membrane peeling and gas filling.

Acupoint catgut embedding therapy is a stimulation method that was developed from traditional acupuncture therapy. It is based on the key principle of acupuncture in traditional Chinese medicine. Especially, it is based on the belief that organ disorders are reflected at specific points on or near the surface of the skin (acupoints). It is also believed that the stimulation of acupoints can modify the physiology of the body. Acupoint catgut embedding therapy employs sutures made of catgut, collagen, or polymer to apply persistent stimulation during suture absorption. This method has been applied extensively in patients with epigastric pain, obesity, low back pain, and leg pain, among others. There are reports of the application of catgut embedding at periocular acupoints for the treatment of myopia. Periocular acupoint catgut embedding is performed by placing 1–2 cm of catgut at the tip of a lumbar puncture needle tube, which is then connected to the needle core after disinfection. The acupuncture penetrates the periocular acupoints to a certain depth, which is usually located in the adipose body of the orbit. The needle core is pushed while the needle tube is withdrawn, and the catgut is embedded in the periocular acupoint. This report describes a unique case of a patient with endophthalmitis with a retained intraocular foreign body (IOFB) after an erroneous periocular acupoint catgut embedding.

突发事件会打乱人们的学习、工作和生活节奏,同时也给医学留学生的教育及临床培训带来了严峻的挑战.在这种情况下,医学远程教育的应用改善了教学过程,提供了更多学习医学课程的机会,扩大了临床实践,对医学生有极大的益处.医学远程教育模式的探索中需要针对目前存在的问题不断改革、完善与创新,开发和使用基于技术及模拟的创新教育模式及方法,提高留学生感知度、易用性以及参与积极性,从而进一步提升教学质量和学习效果,培养合格的医学人才.

Nonsteroidal anti-inflammatory drugs (NSAIDs) are among the most common prescription drugs for inflammation, and topical NSAIDs are often used in ophthalmology to reduce pain, photophobia, inflammation, and edema. In recent years, many published reports have found that NSAIDs play an important role in the treatment of retinal neurodegenerative diseases, such as age-related macular degeneration (AMD), diabetic retinopathy (DR), glaucoma, pathological myopia, and retinitis pigmentosa (RP). The aim of the current review is to provide an overview of the role of various NSAIDs in the treatment of retinal neurodegenerative diseases and the corresponding mechanisms of action. This review highlighted that the topical application of NSAIDs for the treatment of retinal degenerative diseases has been studied to a remarkable extent and that its beneficial effects in many diseases have been proven. In the future, prospective studies with large study populations are required to extend these effects to clinical settings.

Retinal detachment caused by severe ocular trauma is a type of refractory vitreoretinal disease. Current treatment methods include vitrectomy combined with silicone oil tamponade. However, long-term use of silicone oil tamponade has various complications, including a risk of silicone oil dependence that eventually leads to eyeball atrophy and enucleation. Foldable capsular vitreous bodies (FCVBs) offer a good solution for these problems. However, FCVBs have not been used in large-scale clinical applications and few cases have been reported in the published literature. The main use of FCVBs, based on current evidence, is in the treatment of the relatively few (but important) patients whose eyes have no visual potential; the aim of treatment in these patients is globe preservation, rather than restoration of vision. Here, we describe two patients who underwent FCVB implantation. The findings in these patients indicated that FCVBs can effectively support the vitreous cavity and detached retina. FCVB implantation may thus offer a safe and effective method for treatment of severe retinal detachment, avoiding the inconvenience caused by silicone oil dependence and enucleation. To confirm its long-term usefulness in clinical applications, many additional case reports are needed.

Exosomes, small membrane vesicles with a diameter of 30-100 nm, transport lipids, proteins, DNA, and RNA. Exosomes originate from endocytic vessels and are processed and released through exocytosis. They can be taken up by target cells and mediate intercellular communication. Initially, exosomes were thought to be waste products excreted by cells. However, with more research, they have been found to play important roles in physiological and pathological processes. Therefore, they are promising biomarkers for the diagnosis and treatment of a variety of disease conditions, including fundus diseases, ocular surface diseases, retinal diseases, tumors, ocular trauma, and light damage. In this review, we discuss the history, biogenesis, release, isolation, characterization, and biological functions of exosomes, as well as their future application prospects in ophthalmic diseases.

Alcohol intake can cause a wide range of visual system abnormalities. In this study, we characterized how ethanol affects the growth, external morphology and locomotion of zebrafish, particularly with regard to retinal development. Zebrafish embryos were divided into 5 groups and put into hatching liquid for 6 hours. The embryos from 4 groups were treated with varying concentrations of ethanol (0.5%, 1.5%, 2.5% and 3% by volume) from 6 to 24 hours post-fertilization. The toxic effects of ethanol on embryonic development were assessed by mortality, hatching rate and morphologic deformity. The effects of ethanol on locomotive activity were assessed by autonomous motion detection and swimming behavior analysis. The effects of ethanol on retinal morphology were assessed by histologic, immunohistochemical and electron microscopy analyses. Ethanol treatment increased the mortality and induced growth retardation in zebrafish larvae. The locomotive activities of zebrafish embryos/larvae were impeded by exposure to higher (1.5% and 2.5%) concentrations of ethanol. Embryos exposed to higher levels of ethanol at the early developmental stage had a reduction in eye size. The ethanol treatment disrupts the architecture of the retina and reduces retinal size. Embryos exposed to 2.5% concentration of ethanol had morphologic abnormalities of the photoreceptors. Ethanol exposure also inhibited retinal cell differentiation and proliferation, but did not affect apical epithelial polarity. These findings suggest that ethanol affects the growth and external morphology of zebrafish, and higher levels of ethanol exposure can cause defects of locomotor activity and photoreceptor development.

Cytoplasmic dynein is a multi-subunit complex that includes cytoplasmic dynein-1 (dynein1) and cytoplasmic dynein-2 (dynein2). It participates in various basic cellular processes, including nuclear migration, mitotic spindle organization, chromosome separation during mitosis, and the location and function of numerous intracellular organelles. Retinal photoreceptor cells are terminally differentiated neurons that cannot regenerate and cannot be replaced once lost. It is thus crucial to study their development to facilitate the generation and improvement of photoreceptor disease treatments. The outer segment (OS) of photoreceptor cells is a specific sensory cilium. An increasing number of studies have shown that cytoplasmic dynein plays an essential role in the development of retinal photoreceptor cells. To date, people have done a lot of studies on the various functions of dynein in cells and have a very detailed understanding. However, the role of dynein in retinal photoreceptor cells has not been summarized in detail. This article summarizes the currently available knowledge relating to the effects and mechanisms of cytoplasmic dynein on the development and functional maintenance of retinal photoreceptor cells.

Diabetic retinopathy (DR) is a type of retinal microangiopathy caused by diabetes mellitus. It has become the leading cause of blindness among working individuals worldwide. DR is becoming increasingly common among younger diabetic patients and there is a need for lifelong treatment. The pathogenic mechanisms of DR are influenced by a number of factors, such as hyperglycemia, hyperlipidemia, inflammatory response and oxidative stress, among others. Currently, the treatment methods for DR mainly include retinal photocoagulation, vitrectomy, or anti-vascular endothelial growth factor (VEGF) therapy. However, these methods have some disadvantages and limitations. Therefore, it is a matter of great interest and urgency to discover drugs that can target the pathogenesis of DR. Since ancient times, traditional Chinese medicine practitioners have accumulated extensive experiences in the use of Chinese herbal medicine for the prevention and treatment of diseases. In the theory of traditional Chinese medicine, curcumin has the effects of promoting blood circulation and relieving pain. A number of studies have also demonstrated that curcumin has multiple biological activities, including exerting anti-apoptotic, anti-inflammatory, antioxidant and antitumor properties. In recent years, studies have also confirmed that curcumin can prevent a variety of diabetic complications, including diabetic nephropathy (DN). However, the preventive and curative effects of curcumin on DR and its mechanisms of action have not yet been fully elucidated. The present review aimed to explore the therapeutic potential of curcumin in diabetes mellitus and DR.

Background: Methanol toxicity can lead to potentially fatal poisoning. We characterized how methanol affects zebrafish growth, external morphology, and locomotion, paying particular attention to photoreceptor development. Methods: Zebrafish embryos were divided into six groups and placed in hatching liquid for 6 hours. The embryos from five of the six groups were treated with varying concentrations (1%, 2%, 3%, 4%, and 5% by volume) of methanol from 6 to 24 hours post-fertilization. The toxic effects of methanol on zebrafish embryonic development were assessed based on the mortality rate, the hatching rate, and the morphological deformity rate. The effects of methanol on the locomotor activity of zebrafish embryo/larvae were assessed using autonomous motion and swimming behavior analyses. The effects of methanol on photoreceptor development were assessed using electron microscopy analyses. Results: Methanol increases mortality and induces growth retardation in zebrafish embryos. Zebrafish embryos exposed to 3% and 4% methanol during their early embryonic development displayed dramatic decreases in spontaneous tail movement at 24 hours post-fertilization and in the speed of their movement at 120 hours post-fertilization compared with the control group. Embryos exposed to a high (4%) concentration of methanol displayed morphological abnormalities in their photoreceptors. Conclusion: These findings suggest that methanol affects zebrafish growth and external morphology, and higher levels of methanol exposure can cause defects in locomotor activity and photoreceptor development.

Heart failure (HF) is a medical condition inability of the heart to pump sufficient blood to meet the metabolic demand of the body to take place. The number of hospitalized patients with cardiovascular diseases is estimated to be more than 1 million each year, of which 80% to 90% of patients ultimately progress to decompensated HF. Digitalis glycosides exert modest inotropic actions when administered to patients with decompensated HF. Although its efficacy in patients with HF and atrial fibrillation is clear, its value in patients with HF and sinus rhythm has often been questioned. A series of recent studies have cast serious doubt on the benefit of digoxin when added to contemporary HF treatment. We are hypothesizing the role and mechanism of exosome and its biological constituents responsible for worsening the disease state and mortality in decompensated HF patients on digitalis.

Diabetic retinopathy (DR) is a devastating complication of diabetes. The aim of the present study is to investigate the exact role and mechanism of long noncoding RNA MALAT1 (MALAT1) in the progress of DR. An oxygen-induced retinopathy (OIR) mouse model and high glucose (HG) stimulated human retinal microvascular endothelial cells (HRMECs) were employed to mimic the pathological statues of DR. Quantitative real-time PCR (qRT-PCR) and Western blot results showed that MALAT1, VEGFA, and HIF-1α levels were increased in DR retinal tissues and HG-stimulated HRMECs, whereas the expression of miR-203a-3p was decreased. Knockdown of MALAT1 or upregulation of miR-203a-3p both suppressed HG-induced proliferation, migration, and tube formation of HRMECs. A dual-luciferase reporter assay showed that miR-203a-3p could bind to the predicted seed regions of MALAT1 as evidenced by the reduced luciferase activity. Furthermore, enforced downregulation of miR-203a-3p abolished the suppressive effect of MALAT1 silencing on HRMEC cell migration and tube formation. In conclusion, these data demonstrated that MALAT1 may affect angiogenesis by sponging miR-203a-3p in DR, suggesting that MALAT1 may act as a novel therapeutic target for the treatment of DR.

Purpose Human Crb1 is implicated in some forms of retinal degeneration, suggesting a role in photoreceptor maintenance. Multiple Crumbs (Crb) polarity genes are expressed in vertebrate retina, although their functional roles are not well understood. To gain further insight into Crb and photoreceptor maintenance, we compared retinal cell densities between wild-type and Tg(RH2-2:Crb2b-sfEX/RH2-2:GFP)pt108b transgenic zebrafish, in which the extracellular domain of Crb2b-short form (Crb2b-sfEX) is expressed in the retina as a secreted protein, which disrupts the planar organization of RGB cones (red, green, and blue) by interfering with Crb2a/2b-based cone-cone adhesion. Methods We used standard morphometric techniques to assess age-related changes in retinal cell densities in adult zebrafish (3 to 27 months old), and to assess effects of the Crb2b-sfEX transgene on retinal structure and photoreceptor densities. Linear cell densities were measured in all retinal layers in radial sections with JB4-Feulgen histology. Planar (surface) densities of cones were determined in retinal flat-mounts. Cell counts from wild-type and pt108b transgenic fish were compared with both a “photoreceptor maintenance index” and statistical analysis of cell counts. Results Age-related changes in retinal cell linear densities and cone photoreceptor planar densities in wild-type adult zebrafish provided a baseline for analysis. Expression of Crb2b-sfEX caused progressive and selective degeneration of RGB cones, but had no effect on ultraviolet-sensitive (UV) cones, and increased numbers of rod photoreceptors. Conclusions These differential responses of RGB cones, UV cones, and rods to sustained exposure to Crb2b-sfEX suggest that Crb-based photoreceptor maintenance mechanisms are highly selective.