Pub Date : 2025-12-04DOI: 10.1016/j.preteyeres.2025.101421
Christiana Dinah , Marieh Esmaeelpour , Aleksandra V. Rachitskaya , Gabriella De Salvo , Marion R. Munk
There is an unmet need in patients with geographic atrophy (GA) for treatments that preserve and improve functional vision to maintain their independence and quality of life. The limited number of available treatments for GA have demonstrated structural benefits, but none have consistently shown significant functional outcomes in clinical trials. Currently, best-corrected visual acuity (BCVA) is considered the gold standard functional endpoint in clinical trials; however, in the case of GA, it cannot fully evaluate visual impairment or treatment response, particularly in fovea-sparing GA lesions. In addition, BCVA may not fully capture the functional impact of foveal and parafoveal scotomas. There is emerging evidence for the utility of other functional assessments that may provide a more robust representation of the functional impact of GA; however, the current utilization of these tests in GA clinical trials varies widely. This review aims to evaluate current functional endpoints in GA and their strengths and limitations based on characteristics such as strength of structure–function correlation, practicality and feasibility, and patient perspective. There are many factors to consider when choosing a functional vision assessment when designing a GA clinical trial, and each functional vision assessment has several advantages and disadvantages, which are summarized in this review article.
{"title":"Functional endpoints in patients with geographic atrophy: What to consider when designing a clinical trial","authors":"Christiana Dinah , Marieh Esmaeelpour , Aleksandra V. Rachitskaya , Gabriella De Salvo , Marion R. Munk","doi":"10.1016/j.preteyeres.2025.101421","DOIUrl":"10.1016/j.preteyeres.2025.101421","url":null,"abstract":"<div><div>There is an unmet need in patients with geographic atrophy (GA) for treatments that preserve and improve functional vision to maintain their independence and quality of life. The limited number of available treatments for GA have demonstrated structural benefits, but none have consistently shown significant functional outcomes in clinical trials. Currently, best-corrected visual acuity (BCVA) is considered the gold standard functional endpoint in clinical trials; however, in the case of GA, it cannot fully evaluate visual impairment or treatment response, particularly in fovea-sparing GA lesions. In addition, BCVA may not fully capture the functional impact of foveal and parafoveal scotomas. There is emerging evidence for the utility of other functional assessments that may provide a more robust representation of the functional impact of GA; however, the current utilization of these tests in GA clinical trials varies widely. This review aims to evaluate current functional endpoints in GA and their strengths and limitations based on characteristics such as strength of structure–function correlation, practicality and feasibility, and patient perspective. There are many factors to consider when choosing a functional vision assessment when designing a GA clinical trial, and each functional vision assessment has several advantages and disadvantages, which are summarized in this review article.</div></div>","PeriodicalId":21159,"journal":{"name":"Progress in Retinal and Eye Research","volume":"110 ","pages":"Article 101421"},"PeriodicalIF":14.7,"publicationDate":"2025-12-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145689329","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-11-27DOI: 10.1016/j.preteyeres.2025.101420
Yousef A. Fouad , Lorenzo Bianco , Prithvi Ramtohul , Sara Touhami , Rishi Gupta , Saeed Mohammadi , Francesco Bandello , Elisabetta Miserocchi , Lee Merrill Jampol , Maria Vittoria Cicinelli
Multiple Evanescent White Dot Syndrome (MEWDS) is a primary outer retinal inflammatory disorder, classically presenting as an acute, unilateral, self-limiting condition in young to middle-aged adults. It is characterized by multiple small white spots at the posterior pole, foveal granularity, wreath-like hyperfluorescence on fluorescein angiography, and a “dot-over-spot” hypofluorescent pattern on late-phase indocyanine green angiography. This PRISMA-compliant systematic review analyzed 592 eyes from 240 publications, supplemented by an institutional case series. While most cases conformed to the typical phenotype (62 %), nearly one-third were atypical (20 %) or secondary (18 %) to other chorioretinal diseases. Atypical forms included bilateral or recurrent presentations, distinctive angiographic patterns, or absence of spontaneous recovery with permanent structural damage. We also identified a previously unreported phenotype in older adults, featuring confluent hyperautofluorescence extending into the mid-periphery and hyperreflective outer retinal lesions, often with subacute worsening and partial steroid responsiveness. Secondary MEWDS occurred in association with various chorioretinal disorders, most commonly punctate inner choroiditis. Collectively, these findings support viewing MEWDS within the broader spectrum of outer retinal disorders sharing photoreceptor pathology but differing in triggers, imaging signatures, and outcomes. Recognition of atypical and secondary variants is essential for accurate diagnosis, risk stratification, and tailored management.
{"title":"Multiple evanescent white dot syndrome: Typical, atypical, and secondary variants","authors":"Yousef A. Fouad , Lorenzo Bianco , Prithvi Ramtohul , Sara Touhami , Rishi Gupta , Saeed Mohammadi , Francesco Bandello , Elisabetta Miserocchi , Lee Merrill Jampol , Maria Vittoria Cicinelli","doi":"10.1016/j.preteyeres.2025.101420","DOIUrl":"10.1016/j.preteyeres.2025.101420","url":null,"abstract":"<div><div>Multiple Evanescent White Dot Syndrome (MEWDS) is a primary outer retinal inflammatory disorder, classically presenting as an acute, unilateral, self-limiting condition in young to middle-aged adults. It is characterized by multiple small white spots at the posterior pole, foveal granularity, wreath-like hyperfluorescence on fluorescein angiography, and a “dot-over-spot” hypofluorescent pattern on late-phase indocyanine green angiography. This PRISMA-compliant systematic review analyzed 592 eyes from 240 publications, supplemented by an institutional case series. While most cases conformed to the typical phenotype (62 %), nearly one-third were atypical (20 %) or secondary (18 %) to other chorioretinal diseases. Atypical forms included bilateral or recurrent presentations, distinctive angiographic patterns, or absence of spontaneous recovery with permanent structural damage. We also identified a previously unreported phenotype in older adults, featuring confluent hyperautofluorescence extending into the mid-periphery and hyperreflective outer retinal lesions, often with subacute worsening and partial steroid responsiveness. Secondary MEWDS occurred in association with various chorioretinal disorders, most commonly punctate inner choroiditis. Collectively, these findings support viewing MEWDS within the broader spectrum of outer retinal disorders sharing photoreceptor pathology but differing in triggers, imaging signatures, and outcomes. Recognition of atypical and secondary variants is essential for accurate diagnosis, risk stratification, and tailored management.</div></div>","PeriodicalId":21159,"journal":{"name":"Progress in Retinal and Eye Research","volume":"110 ","pages":"Article 101420"},"PeriodicalIF":14.7,"publicationDate":"2025-11-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145611702","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-11-24DOI: 10.1016/j.preteyeres.2025.101417
Indumathi Singh , Ann M. Poynten , Arun V. Krishnan , Mark D.P. Willcox , Maria Markoulli
Type 2 diabetes is a chronic, systemic, metabolic disorder characterized by persistent hyperglycemia and associated with a broad spectrum of complications, including those affecting the ocular surface. This article reviews the structural, biochemical, and neuropathic changes observed in the ocular surface of patients with diabetes. Hyperglycemia and associated metabolic imbalances lead to tear film instability, inflammation, oxidative stress, and peripheral neuropathy, contributing to the pathogenesis of dry eye disease, impaired corneal wound healing and corneal neuropathy. In addition, systemic factors such as glycemic control, inflammatory cytokines, and microvascular impairment have direct impact on ocular surface homeostasis. This review also evaluates the effects of antidiabetic therapies on the ocular surface. Recent studies suggest that drugs such as metformin, sodium-glucose co-transporter 2 inhibitors, glucagon like peptide-1 receptor agonists, and insulin along with glucose control, may offer the ocular surface protective benefits. Evidence supports their roles in reducing ocular surface inflammation, promoting corneal nerve regeneration, and improving tear film homeostasis. A comprehensive understanding of these factors may facilitate improved screening, early diagnosis, and integrative management of ocular surface disorders in type 2 diabetes.
{"title":"The ocular surface in type 2 diabetes: pathophysiology and impact of anti-diabetic drugs","authors":"Indumathi Singh , Ann M. Poynten , Arun V. Krishnan , Mark D.P. Willcox , Maria Markoulli","doi":"10.1016/j.preteyeres.2025.101417","DOIUrl":"10.1016/j.preteyeres.2025.101417","url":null,"abstract":"<div><div>Type 2 diabetes is a chronic, systemic, metabolic disorder characterized by persistent hyperglycemia and associated with a broad spectrum of complications, including those affecting the ocular surface. This article reviews the structural, biochemical, and neuropathic changes observed in the ocular surface of patients with diabetes. Hyperglycemia and associated metabolic imbalances lead to tear film instability, inflammation, oxidative stress, and peripheral neuropathy, contributing to the pathogenesis of dry eye disease, impaired corneal wound healing and corneal neuropathy. In addition, systemic factors such as glycemic control, inflammatory cytokines, and microvascular impairment have direct impact on ocular surface homeostasis. This review also evaluates the effects of antidiabetic therapies on the ocular surface. Recent studies suggest that drugs such as metformin, sodium-glucose co-transporter 2 inhibitors, glucagon like peptide-1 receptor agonists, and insulin along with glucose control, may offer the ocular surface protective benefits. Evidence supports their roles in reducing ocular surface inflammation, promoting corneal nerve regeneration, and improving tear film homeostasis. A comprehensive understanding of these factors may facilitate improved screening, early diagnosis, and integrative management of ocular surface disorders in type 2 diabetes.</div></div>","PeriodicalId":21159,"journal":{"name":"Progress in Retinal and Eye Research","volume":"110 ","pages":"Article 101417"},"PeriodicalIF":14.7,"publicationDate":"2025-11-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145592820","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-11-22DOI: 10.1016/j.preteyeres.2025.101418
Elisa Landi , Derick G. Wansink , Vanessa LaPointe , Hans van Bokhoven , Alice E. Davidson , Mor Dickman
Fuchs endothelial corneal dystrophy (FECD) is a heritable disorder distinguished by a progressive degeneration of the corneal endothelium. In its late-onset form, FECD has been associated with a trinucleotide repeat (TNR) expansion (CTG18.1) located in an intronic region of the TCF4 gene, whose frequency is variable among different ancestry groups. Since its discovery, studies investigating CTG18.1-mediated pathogenesis have steadily increased, yet much concerning the unique and tissue-specific clinical features of the disease, as well as its heritable mode of transmission, remain poorly understood. The field of repeat expansion disorders has greatly informed mechanistic understanding of CTG18.1-mediated FECD. In particular, molecular mechanisms underlying myotonic dystrophy type 1, attributed to a CTG expansion in the 3ˈ UTR of the DMPK gene, have considerably informed the FECD field, despite its stark contrast in terms of multisystemic manifestations and variable age at onset. In this work, we critically discuss the non-mutually shared pathogenic parallelisms existing between the pathologies, as well as the unique molecular signatures exhibited by FECD and DM1, speculating on potential research directions for future investigations. Moreover, we discuss the few studies published over the past decade describing the occurrence of FECD in DM1 patients. Here, we debate possible shared molecular signatures that could explain FECD development as a consequence of a non-coding CTG expansion, irrespective of loci (e.g. DMPK or TCF4), and discuss experimental approaches to explain whether these pathologies share toxic mechanisms that arise from these distinct repeat elements.
{"title":"Pathological mechanism in Fuchs endothelial corneal dystrophy and myotonic dystrophy type 1: more than meets the eye","authors":"Elisa Landi , Derick G. Wansink , Vanessa LaPointe , Hans van Bokhoven , Alice E. Davidson , Mor Dickman","doi":"10.1016/j.preteyeres.2025.101418","DOIUrl":"10.1016/j.preteyeres.2025.101418","url":null,"abstract":"<div><div>Fuchs endothelial corneal dystrophy (FECD) is a heritable disorder distinguished by a progressive degeneration of the corneal endothelium. In its late-onset form, FECD has been associated with a trinucleotide repeat (TNR) expansion (CTG18.1) located in an intronic region of the <em>TCF4</em> gene, whose frequency is variable among different ancestry groups. Since its discovery, studies investigating CTG18.1-mediated pathogenesis have steadily increased, yet much concerning the unique and tissue-specific clinical features of the disease, as well as its heritable mode of transmission, remain poorly understood. The field of repeat expansion disorders has greatly informed mechanistic understanding of CTG18.1-mediated FECD. In particular, molecular mechanisms underlying myotonic dystrophy type 1, attributed to a CTG expansion in the 3ˈ UTR of the <em>DMPK</em> gene, have considerably informed the FECD field, despite its stark contrast in terms of multisystemic manifestations and variable age at onset. In this work, we critically discuss the non-mutually shared pathogenic parallelisms existing between the pathologies, as well as the unique molecular signatures exhibited by FECD and DM1, speculating on potential research directions for future investigations. Moreover, we discuss the few studies published over the past decade describing the occurrence of FECD in DM1 patients. Here, we debate possible shared molecular signatures that could explain FECD development as a consequence of a non-coding CTG expansion, irrespective of loci (e.g. <em>DMPK</em> or <em>TCF4</em>), and discuss experimental approaches to explain whether these pathologies share toxic mechanisms that arise from these distinct repeat elements.</div></div>","PeriodicalId":21159,"journal":{"name":"Progress in Retinal and Eye Research","volume":"110 ","pages":"Article 101418"},"PeriodicalIF":14.7,"publicationDate":"2025-11-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145575514","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-11-17DOI: 10.1016/j.preteyeres.2025.101416
Xuran Duan , Chaoyu Lei , Chris Hong Long Lim , Jianbin Ding , Jodhbir S. Mehta , Sayan Basu , Luke Johnston , Yujie Ren , Chen Zhao , Victor Koh Teck Chang , Huifang Zhou
The conjunctival blood vessels are the only microcirculatory system on the body surface that can be observed non-invasively. Anatomically interconnected with multiple craniofacial circulatory systems, these vessels can indirectly reflect the blood supply to these areas and the overall state of systemic microcirculation. We synthesize findings from 48 studies spanning 2020–2025. Overall, existing research has found that the conjunctival vascular parameters can change in various diseases such as diabetes, cardiovascular diseases, and autoimmune diseases, and may even precede organic lesions. Recent advancements in conjunctival vessel imaging and analysis technologies have enabled the identification and evaluation of various ocular and systemic diseases based on conjunctival vascular parameters. However, existing studies are limited by insufficient sample sizes, covariate interference, limited disease types, a lack of investigation into the underlying mechanisms of conjunctival vascular changes, and inadequate integration with emerging technologies, such as artificial intelligence. Future research should aim to broaden the scope of investigation, delve deeper into the mechanisms governing conjunctival vascular alterations, and integrate artificial intelligence to establish a solid foundation for the clinical application of conjunctival vascular parameters.
{"title":"Quantitative analysis of conjunctival vascular alterations: Applications in ocular and systemic disease detection","authors":"Xuran Duan , Chaoyu Lei , Chris Hong Long Lim , Jianbin Ding , Jodhbir S. Mehta , Sayan Basu , Luke Johnston , Yujie Ren , Chen Zhao , Victor Koh Teck Chang , Huifang Zhou","doi":"10.1016/j.preteyeres.2025.101416","DOIUrl":"10.1016/j.preteyeres.2025.101416","url":null,"abstract":"<div><div>The conjunctival blood vessels are the only microcirculatory system on the body surface that can be observed non-invasively. Anatomically interconnected with multiple craniofacial circulatory systems, these vessels can indirectly reflect the blood supply to these areas and the overall state of systemic microcirculation. We synthesize findings from 48 studies spanning 2020–2025. Overall, existing research has found that the conjunctival vascular parameters can change in various diseases such as diabetes, cardiovascular diseases, and autoimmune diseases, and may even precede organic lesions. Recent advancements in conjunctival vessel imaging and analysis technologies have enabled the identification and evaluation of various ocular and systemic diseases based on conjunctival vascular parameters. However, existing studies are limited by insufficient sample sizes, covariate interference, limited disease types, a lack of investigation into the underlying mechanisms of conjunctival vascular changes, and inadequate integration with emerging technologies, such as artificial intelligence. Future research should aim to broaden the scope of investigation, delve deeper into the mechanisms governing conjunctival vascular alterations, and integrate artificial intelligence to establish a solid foundation for the clinical application of conjunctival vascular parameters.</div></div>","PeriodicalId":21159,"journal":{"name":"Progress in Retinal and Eye Research","volume":"110 ","pages":"Article 101416"},"PeriodicalIF":14.7,"publicationDate":"2025-11-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145553612","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-11-11DOI: 10.1016/j.preteyeres.2025.101414
Zuyi Yang , Wenfei Zhang , Xingwang Gu , Xinyu Zhao , SriniVas R. Sadda , Gemmy Cheung , Adrian Koh , Anat Loewenstein , Bing Li , Chuting Wang , Jiaqi Zhang , Jingyuan Yang , Kehan Jin , Lihui Meng , Lulu Chen , Meiqian He , Minzhen Yuan , Mingyue Luo , Nien Li , Paisan Ruamviboonsuk , Youxin Chen
Polypoidal choroidal vasculopathy (PCV) is an ocular condition predominantly affecting elderly individuals of Asian descent, characterized by the presence of polypoidal lesions and branching neovascular networks in the sub-retinal pigment epithelium (RPE) space. It has garnered increased attention for its potential differences from neovascular age-related macular degeneration. Genetic studies have identified specific genetic markers associated with PCV. Advances in imaging techniques, particularly optical coherence tomography (OCT) and OCT angiography, have significantly enhanced the diagnosis of PCV and our insight into its unique pathogenesis. Treatment strategies for PCV have evolved, with anti-vascular endothelial growth factor (VEGF) monotherapy becoming the primary treatment, and combination therapies including photodynamic therapy showing promising results. Consideration of targets beyond VEGF and the incorporation of artificial intelligence (AI) based analysis strategies may open the door to more personalized, precise, and effective treatments for patients. This review comprehensively discusses the current knowledge and recent advancements in PCV, including its epidemiology, genetics, biomarkers, pathogenesis, diagnosis, and management. It also highlights the need to explore mechanism underlying the higher prevalence of PCV in pigmented races, clarify the roles of pachychoroid and pachydrusen in PCV pathogenesis, and develop animal models that can better recapitulate the disease's pathological features.
{"title":"Polypoidal choroidal vasculopathy: In-depth insights and promising future directions","authors":"Zuyi Yang , Wenfei Zhang , Xingwang Gu , Xinyu Zhao , SriniVas R. Sadda , Gemmy Cheung , Adrian Koh , Anat Loewenstein , Bing Li , Chuting Wang , Jiaqi Zhang , Jingyuan Yang , Kehan Jin , Lihui Meng , Lulu Chen , Meiqian He , Minzhen Yuan , Mingyue Luo , Nien Li , Paisan Ruamviboonsuk , Youxin Chen","doi":"10.1016/j.preteyeres.2025.101414","DOIUrl":"10.1016/j.preteyeres.2025.101414","url":null,"abstract":"<div><div>Polypoidal choroidal vasculopathy (PCV) is an ocular condition predominantly affecting elderly individuals of Asian descent, characterized by the presence of polypoidal lesions and branching neovascular networks in the sub-retinal pigment epithelium (RPE) space. It has garnered increased attention for its potential differences from neovascular age-related macular degeneration. Genetic studies have identified specific genetic markers associated with PCV. Advances in imaging techniques, particularly optical coherence tomography (OCT) and OCT angiography, have significantly enhanced the diagnosis of PCV and our insight into its unique pathogenesis. Treatment strategies for PCV have evolved, with anti-vascular endothelial growth factor (VEGF) monotherapy becoming the primary treatment, and combination therapies including photodynamic therapy showing promising results. Consideration of targets beyond VEGF and the incorporation of artificial intelligence (AI) based analysis strategies may open the door to more personalized, precise, and effective treatments for patients. This review comprehensively discusses the current knowledge and recent advancements in PCV, including its epidemiology, genetics, biomarkers, pathogenesis, diagnosis, and management. It also highlights the need to explore mechanism underlying the higher prevalence of PCV in pigmented races, clarify the roles of pachychoroid and pachydrusen in PCV pathogenesis, and develop animal models that can better recapitulate the disease's pathological features.</div></div>","PeriodicalId":21159,"journal":{"name":"Progress in Retinal and Eye Research","volume":"110 ","pages":"Article 101414"},"PeriodicalIF":14.7,"publicationDate":"2025-11-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145498695","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-11-01DOI: 10.1016/j.preteyeres.2025.101411
MD Imam Uddin
Oxygen is the major element for metabolism in the retina. Reduced oxygen supply causes significant changes in cellular metabolism and gene expression in the retina initiating inflammasome activation, apoptosis of retinal cells, mitochondrial damage, oxidative stress and neurodegeneration. Physiologically, retinal hypoxia plays important role regulating vasculogenesis during our development in early life. Retinal hypoxia also plays key regulatory roles during the onset and progression of many retinopathy conditions including neovascularization at later stages of our life. Though the exact mechanism of neovascularization is still largely unknown, hypoxia may contribute to the over expression of vascular endothelial growth factor (VEGF), and VEGF is a known inducer of neovascularization. Thus, molecular imaging of retinal hypoxia could be an important diagnostic tool assessing the risk of retinopathy, its progression, and response to therapy. Imaging retinal hypoxia is also an important diagnostic tool assessing the risk of inflammasome activation, mitochondrial damage, oxidative stress and apoptosis of retinal cells at molecular levels. This review will provide an overview of technologies to detect retinal hypoxia in the living retinal tissues before the onset of tissue damage. This review will also discuss the design and development of HYPOX-4, a highly sensitive molecular imaging probe capable of detecting retinal hypoxia in the living retina before the onset of neovascularization. The author will further discuss a quantitative method to assess HYPOX-4 fluorescence intensity measurement by computational methods, correlating with levels of retinal hypoxia and create a predictive biomarker for retinal neovascularization. An overview of the technology development will also include Dr. Linsenmeier's early development of microelectrode for our fundamental understanding of retinal tissue oxygenation using an invasive measurement technique. An overview of the other emerging technologies, including retinal oximetry, phosphorescence lifetime imaging and photoacoustic imaging will be discussed.
{"title":"Imaging of the retinal hypoxia: A journey from oxygen microelectrode to the first hypoxia imaging in the living retina","authors":"MD Imam Uddin","doi":"10.1016/j.preteyeres.2025.101411","DOIUrl":"10.1016/j.preteyeres.2025.101411","url":null,"abstract":"<div><div>Oxygen is the major element for metabolism in the retina. Reduced oxygen supply causes significant changes in cellular metabolism and gene expression in the retina initiating inflammasome activation, apoptosis of retinal cells, mitochondrial damage, oxidative stress and neurodegeneration. Physiologically, retinal hypoxia plays important role regulating vasculogenesis during our development in early life. Retinal hypoxia also plays key regulatory roles during the onset and progression of many retinopathy conditions including neovascularization at later stages of our life. Though the exact mechanism of neovascularization is still largely unknown, hypoxia may contribute to the over expression of vascular endothelial growth factor (VEGF), and VEGF is a known inducer of neovascularization. Thus, molecular imaging of retinal hypoxia could be an important diagnostic tool assessing the risk of retinopathy, its progression, and response to therapy. Imaging retinal hypoxia is also an important diagnostic tool assessing the risk of inflammasome activation, mitochondrial damage, oxidative stress and apoptosis of retinal cells at molecular levels. This review will provide an overview of technologies to detect retinal hypoxia in the living retinal tissues before the onset of tissue damage. This review will also discuss the design and development of HYPOX-4, a highly sensitive molecular imaging probe capable of detecting retinal hypoxia in the living retina before the onset of neovascularization. The author will further discuss a quantitative method to assess HYPOX-4 fluorescence intensity measurement by computational methods, correlating with levels of retinal hypoxia and create a predictive biomarker for retinal neovascularization. An overview of the technology development will also include Dr. Linsenmeier's early development of microelectrode for our fundamental understanding of retinal tissue oxygenation using an invasive measurement technique. An overview of the other emerging technologies, including retinal oximetry, phosphorescence lifetime imaging and photoacoustic imaging will be discussed.</div></div>","PeriodicalId":21159,"journal":{"name":"Progress in Retinal and Eye Research","volume":"109 ","pages":"Article 101411"},"PeriodicalIF":14.7,"publicationDate":"2025-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145383788","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-11-01DOI: 10.1016/j.preteyeres.2025.101410
Jason C. Yam , Xiu Juan Zhang , Ebenezer Zaabaar , Yuyao Wang , Yuelan Gao , Yuzhou Zhang , Xiaotong Li , Ka Wai Kam , Fangyao Tang , Wai Kit Chu , Xiangtian Zhou , Wei Zhang , Xiangui He , Pei-Chang Wu , Kathryn A. Rose , Ian Morgan , Mingguang He , Kyoko Ohno-Matsui , Jost B. Jonas , Mingzhi Zhang , Chi Pui Pang
The alarming increase in childhood myopia has emerged as a significant public health concern. Due to its long-term consequences, there is also an expanding interest in adult-onset myopia. This review provides a comprehensive summary of interventions for slowing the onset and progression of myopia and discusses factors influencing their efficacy. Outdoor time is an effective intervention for at-risk pre-myopes, which can reduce myopia onset by up to 50 % and has been implemented on a large scale in some countries through school reforms. 0.05 % atropine and repeated low-level red light (RLRL) have also shown the potential to prevent myopia onset by approximately 50 %, though the cost-benefit of implementing them on a large scale warrants more research. Low-concentration atropine, various designs of peripheral defocus spectacles, contact lenses, and RLRL effectively slow myopia progression by at least 50 %. A history of higher baseline myopia status, faster baseline progression, parental myopia, high-risk lifestyle, and less outdoor time requires rigorous interventions. When combined with RLRL or atropine concentrations higher than 0.025 %, orthokeratology significantly improves myopia control in fast progressors and/or high myopes. Combining low-concentration atropine with peripheral defocus glasses or dual-focus contact lenses also yields better efficacy than monotherapy. There is limited research on adult myopia control, but offering comprehensive lifestyle and visual environment recommendations remains essential. Consistent use of these interventions and thorough safety monitoring are crucial for building clinical confidence. The success of myopia control hinges on personalization, given the diverse factors influencing efficacy and the challenges of large-scale implementation.
{"title":"Interventions to reduce incidence and progression of myopia in children and adults","authors":"Jason C. Yam , Xiu Juan Zhang , Ebenezer Zaabaar , Yuyao Wang , Yuelan Gao , Yuzhou Zhang , Xiaotong Li , Ka Wai Kam , Fangyao Tang , Wai Kit Chu , Xiangtian Zhou , Wei Zhang , Xiangui He , Pei-Chang Wu , Kathryn A. Rose , Ian Morgan , Mingguang He , Kyoko Ohno-Matsui , Jost B. Jonas , Mingzhi Zhang , Chi Pui Pang","doi":"10.1016/j.preteyeres.2025.101410","DOIUrl":"10.1016/j.preteyeres.2025.101410","url":null,"abstract":"<div><div>The alarming increase in childhood myopia has emerged as a significant public health concern. Due to its long-term consequences, there is also an expanding interest in adult-onset myopia. This review provides a comprehensive summary of interventions for slowing the onset and progression of myopia and discusses factors influencing their efficacy. Outdoor time is an effective intervention for at-risk pre-myopes, which can reduce myopia onset by up to 50 % and has been implemented on a large scale in some countries through school reforms. 0.05 % atropine and repeated low-level red light (RLRL) have also shown the potential to prevent myopia onset by approximately 50 %, though the cost-benefit of implementing them on a large scale warrants more research. Low-concentration atropine, various designs of peripheral defocus spectacles, contact lenses, and RLRL effectively slow myopia progression by at least 50 %. A history of higher baseline myopia status, faster baseline progression, parental myopia, high-risk lifestyle, and less outdoor time requires rigorous interventions. When combined with RLRL or atropine concentrations higher than 0.025 %, orthokeratology significantly improves myopia control in fast progressors and/or high myopes. Combining low-concentration atropine with peripheral defocus glasses or dual-focus contact lenses also yields better efficacy than monotherapy. There is limited research on adult myopia control, but offering comprehensive lifestyle and visual environment recommendations remains essential. Consistent use of these interventions and thorough safety monitoring are crucial for building clinical confidence. The success of myopia control hinges on personalization, given the diverse factors influencing efficacy and the challenges of large-scale implementation.</div></div>","PeriodicalId":21159,"journal":{"name":"Progress in Retinal and Eye Research","volume":"109 ","pages":"Article 101410"},"PeriodicalIF":14.7,"publicationDate":"2025-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145318493","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-11-01DOI: 10.1016/j.preteyeres.2025.101415
Chen-Wei Pan , Xing-Xuan Dong , Carla Lanca , Yining Wang , Seang-Mei Saw , Xiangui He , Dan-Ning Hu , Qiao Fan , Andrzej Grzybowski , Kyoko Ohno-Matsui
The global prevalence of myopia and pathologic myopia (PM) has dramatically increased, raising significant public health concerns due to associated vision-threatening complications, such as myopic maculopathy (MM). This comprehensive review integrates the latest evidence regarding the environmental, genetic, and epigenetic factors contributing to myopia, as well as recent advances in precision medicine and therapeutic approaches aimed at mitigating the disease's impact. We examine how environmental factors interact with polygenic risk factors and epigenetic changes to influence disease progression. The application of artificial intelligence (AI) enhances the integration of genomic, environmental, and clinical data, thereby improving risk assessment and personalizing treatment options. Therapeutic strategies, including the use of low-dose atropine, orthokeratology, and repeated low-level red-light therapy, have shown promise in controlling myopia. Furthermore, emerging gene-editing techniques are being developed, although they are unlikely to be implemented as treatments for myopia and PM in the near future. Despite these advancements, disparities in resource availability and the implementation of interventions continue to hinder global equity, underscoring the need for scalable solutions such as mobile health applications and community-based preventive programs. This review emphasizes the importance of interdisciplinary collaboration to merge precision medicine with public health strategies, ensuring that scientific breakthroughs are equitably translated into clinical care. By aligning environmental preventive measures, genetic discoveries, and AI-powered innovations, this review outlines a strategic plan for reducing the global burden of myopia and its complications.
{"title":"Global perspectives on myopia and pathologic myopia: From environmental drivers to precision medicine","authors":"Chen-Wei Pan , Xing-Xuan Dong , Carla Lanca , Yining Wang , Seang-Mei Saw , Xiangui He , Dan-Ning Hu , Qiao Fan , Andrzej Grzybowski , Kyoko Ohno-Matsui","doi":"10.1016/j.preteyeres.2025.101415","DOIUrl":"10.1016/j.preteyeres.2025.101415","url":null,"abstract":"<div><div>The global prevalence of myopia and pathologic myopia (PM) has dramatically increased, raising significant public health concerns due to associated vision-threatening complications, such as myopic maculopathy (MM). This comprehensive review integrates the latest evidence regarding the environmental, genetic, and epigenetic factors contributing to myopia, as well as recent advances in precision medicine and therapeutic approaches aimed at mitigating the disease's impact. We examine how environmental factors interact with polygenic risk factors and epigenetic changes to influence disease progression. The application of artificial intelligence (AI) enhances the integration of genomic, environmental, and clinical data, thereby improving risk assessment and personalizing treatment options. Therapeutic strategies, including the use of low-dose atropine, orthokeratology, and repeated low-level red-light therapy, have shown promise in controlling myopia. Furthermore, emerging gene-editing techniques are being developed, although they are unlikely to be implemented as treatments for myopia and PM in the near future. Despite these advancements, disparities in resource availability and the implementation of interventions continue to hinder global equity, underscoring the need for scalable solutions such as mobile health applications and community-based preventive programs. This review emphasizes the importance of interdisciplinary collaboration to merge precision medicine with public health strategies, ensuring that scientific breakthroughs are equitably translated into clinical care. By aligning environmental preventive measures, genetic discoveries, and AI-powered innovations, this review outlines a strategic plan for reducing the global burden of myopia and its complications.</div></div>","PeriodicalId":21159,"journal":{"name":"Progress in Retinal and Eye Research","volume":"109 ","pages":"Article 101415"},"PeriodicalIF":14.7,"publicationDate":"2025-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145531189","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-11-01DOI: 10.1016/j.preteyeres.2025.101412
Mario R. Romano , Mariantonia Ferrara , Peter Szurman , Angelo Spadaro , Hannah J Levis , Andrea Govetto , Tommaso Rossi , Chiara BM. Platania , Kai Januschowski , Claudio Bucolo , Vito Romano
Over the last decade, vital dyes have revolutionized ophthalmic surgery, becoming indispensable tools in many intraocular procedures. These intraocular medical devices enhance visualization, facilitate tissue differentiation and improve surgical precision, ultimately optimizing outcomes. An understanding of their physicochemical properties and staining patterns is crucial for maximizing their benefits and achieving near-histological accuracy. In the recent years, increasing attention has been given to the biocompatibility of intraocular devices to enhance safety and minimise risks. Despite their widespread use, the long-term safety, interactions with intraocular devices, and optimal staining protocols of vital dyes remain insufficiently understood. Addressing these gaps is critical to improving surgical efficacy and patient safety. This review synthesizes recent findings to bridge these knowledge gaps and provide updated clinical insights, offering a comprehensive and detailed analysis of the physicochemical properties, staining mechanisms, and safety profiles of both traditional and newly developed vital dyes. Additionally, it examines how these properties influence surgical efficacy and biocompatibility. We also present an in-depth overview of experimental and clinical studies investigating the potential intraocular toxicity of vital dyes, focusing on crucial and controversial topics, such as surgical risk factors, the interaction between intraocular medical devices and the role of phototoxicity. Drawing on the latest experimental and clinical evidence, we propose updated guidelines to optimise the safe and effective use of vital dyes in intraocular surgery and patients outcomes.
{"title":"Safety and effectiveness of vital dyes for intraocular surgery","authors":"Mario R. Romano , Mariantonia Ferrara , Peter Szurman , Angelo Spadaro , Hannah J Levis , Andrea Govetto , Tommaso Rossi , Chiara BM. Platania , Kai Januschowski , Claudio Bucolo , Vito Romano","doi":"10.1016/j.preteyeres.2025.101412","DOIUrl":"10.1016/j.preteyeres.2025.101412","url":null,"abstract":"<div><div>Over the last decade, vital dyes have revolutionized ophthalmic surgery, becoming indispensable tools in many intraocular procedures. These intraocular medical devices enhance visualization, facilitate tissue differentiation and improve surgical precision, ultimately optimizing outcomes. An understanding of their physicochemical properties and staining patterns is crucial for maximizing their benefits and achieving near-histological accuracy. In the recent years, increasing attention has been given to the biocompatibility of intraocular devices to enhance safety and minimise risks. Despite their widespread use, the long-term safety, interactions with intraocular devices, and optimal staining protocols of vital dyes remain insufficiently understood. Addressing these gaps is critical to improving surgical efficacy and patient safety. This review synthesizes recent findings to bridge these knowledge gaps and provide updated clinical insights, offering a comprehensive and detailed analysis of the physicochemical properties, staining mechanisms, and safety profiles of both traditional and newly developed vital dyes. Additionally, it examines how these properties influence surgical efficacy and biocompatibility. We also present an in-depth overview of experimental and clinical studies investigating the potential intraocular toxicity of vital dyes, focusing on crucial and controversial topics, such as surgical risk factors, the interaction between intraocular medical devices and the role of phototoxicity. Drawing on the latest experimental and clinical evidence, we propose updated guidelines to optimise the safe and effective use of vital dyes in intraocular surgery and patients outcomes.</div></div>","PeriodicalId":21159,"journal":{"name":"Progress in Retinal and Eye Research","volume":"110 ","pages":"Article 101412"},"PeriodicalIF":14.7,"publicationDate":"2025-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145412271","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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