Progress in Retinal and Eye Research最新文献

{"title":"Retinal vessel imaging in inflammatory disease: From endothelial dysfunction to clinical evidence and translation.","authors":"Timon Wallraven, Roman Günthner, Andrea Ribeiro, Momin Alnemer, Konstantin Kotliar, Maciej Lech, Nathalie Bleidißel, Rebecca Wicklein, Christoph Hauser, Lukas Streese, Martin J Menten, Henner Hanssen, Christoph Schmaderer","doi":"10.1016/j.preteyeres.2026.101472","DOIUrl":"10.1016/j.preteyeres.2026.101472","url":null,"abstract":"<p><p>Inflammatory processes drive a heterogeneous spectrum of diseases, including cardiovascular (CV), neurodegenerative, autoimmune, rare, and viral disorders, which together account for a major global disease burden. Despite diverse clinical manifestations, these conditions share systemic endothelial dysfunction (ED) as a common pathophysiological hallmark. The retina, accessible through non-invasive imaging, provides a unique window into systemic microvascular health. Over the past decades, retinal vessel analysis (RVA), both static and dynamic, has emerged as a robust tool for detecting and predicting microvascular alterations in inflammatory diseases. Large population-based cohorts, including the Atherosclerosis Risk in Communities (ARIC, n > 9000 participants) study and the Rotterdam Study (n > 5000), have shown that retinal diameter changes independently predict incident CV events and all-cause mortality. Recent UK Biobank (n > 45,000) analyses further demonstrate incremental value in stroke prediction beyond traditional risk factors (AUC 0.739 to 0.752; p < 0.001). Other retinal imaging modalities, such as optical coherence tomography angiography (OCTA) and adaptive optics (AO), provide complementary high-resolution structural data on capillary architecture and perfusion integrity. The retinal vascular phenotype reflects both shared and disease-specific mechanisms of ED. Therefore, accurate interpretation of retinal biomarkers requires an understanding of the molecular pathways that shape ED across disease entities, thereby forming the conceptual foundation of oculomics. We synthesize current evidence linking systemic ED to retinal microvascular structure and function across major categories of inflammatory disease. We integrate findings from static and dynamic RVA, OCTA, and AO, discuss their mechanistic interpretation within the emerging framework of oculomics, and critically evaluate challenges for clinical translation. Finally, we outline how artificial intelligence (AI) may facilitate robust, scalable implementation of retinal biomarkers for risk stratification, disease monitoring, and outcome prediction. This review moves beyond modality-specific descriptions to propose a unified biological and translational framework for retinal biomarkers.</p>","PeriodicalId":21159,"journal":{"name":"Progress in Retinal and Eye Research","volume":" ","pages":"101472"},"PeriodicalIF":14.7,"publicationDate":"2026-05-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147842297","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}

{"title":"Minimally invasive glaucoma surgery in the surgical landscape of primary angle closure glaucoma: Current innovations and future trends","authors":"Fei Li ,&nbsp;Fengbin Lin ,&nbsp;Zefeng Yang ,&nbsp;Fengqi Zhou ,&nbsp;Yunhe Song ,&nbsp;Clement C. Tham ,&nbsp;Ki Ho Park ,&nbsp;Tin Aung ,&nbsp;Tanuj Dada ,&nbsp;Robert N. Weinreb ,&nbsp;Dennis S.C. Lam ,&nbsp;Xiulan Zhang","doi":"10.1016/j.preteyeres.2026.101470","DOIUrl":"10.1016/j.preteyeres.2026.101470","url":null,"abstract":"<div><div>Primary angle-closure glaucoma (PACG) is a major cause of irreversible blindness worldwide, with the highest burden in Asia. Its pathogenesis involves the interplay of multiple mechanisms, including pupillary block, plateau iris configuration, lens-related crowding, and dynamic choroidal expansion. Traditional surgical management has relied on trabeculectomy, lens extraction, or transscleral cyclophotocoagulation, which often achieve substantial intraocular pressure (IOP) control but carry significant risks and require prolonged recovery.</div><div>Minimally invasive glaucoma surgery (MIGS) expands treatment options for PACG once angle access is restored. It offers safer, earlier, and targeted interventions tailored to the underlying mechanisms. Techniques range from trabecular meshwork (TM) and Schlemm's canal–based procedures to subconjunctival stents and ciliary body approaches. Combined with lens extraction, these methods deepen the anterior chamber, release peripheral anterior synechiae, and restore physiological outflow, with clinical evidence showing 20-50% IOP reductions and reduced medication burden.</div><div>This paper reviews anatomical, physiological, and clinical evidence for the use of MIGS in PACG, discussing how these procedures can complement, or in selected cases replace, invasive filtration surgery, potentially enabling earlier intervention while maintaining a favorable safety profile. Future advancements will hinge on device refinements for narrow-angle eyes, imaging-guided precision, biologic modulation, and strategies to enhance cost-effectiveness and accessibility, ultimately enabling individualized, mechanism-based treatment pathways.</div></div>","PeriodicalId":21159,"journal":{"name":"Progress in Retinal and Eye Research","volume":"112 ","pages":"Article 101470"},"PeriodicalIF":14.7,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147779731","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}

{"title":"Are Müller Glial Cells Gatekeepers of Neuroprotection and Regeneration in Age-Related Macular Degeneration? Unraveling Their Roles in Pathophysiology and Therapeutic Innovation","authors":"Kai-Yang Chen, Hoi-Chun Chan, Yih-Shiou Hwang, Wan-Wan Lin, Chi-Ming Chan MD PhD","doi":"10.1016/j.preteyeres.2026.101471","DOIUrl":"https://doi.org/10.1016/j.preteyeres.2026.101471","url":null,"abstract":"Age-related macular degeneration (AMD) is traditionally conceptualized as a disorder of the retinal pigment epithelium (RPE)–photoreceptor axis; however, this paradigm incompletely explains early disease dynamics and therapeutic failure in geographic atrophy (GA). This review aims to redefine AMD progression through a Müller glial cell-centered framework that integrates cellular homeostasis, structural transitions, and stage-dependent therapeutic implications. Emerging transcriptomic, histologic, and functional evidence demonstrates that Müller glial cells actively participate in AMD pathobiology, including complement regulation, metabolic coupling, redox control, and inflammatory signaling. In early AMD, Müller glial cells exhibit adaptive responses that preserve retinal integrity despite increasing metabolic and extracellular stress. Progressive accumulation of basal laminar deposits and extracellular remodeling imposes diffusion constraints and inflammatory burden, promoting glial reprogramming. A critical transition occurs at external limiting membrane (ELM) descent, which corresponds to loss of photoreceptor support, disruption of retinal compartmentalization, and onset of irreversible degeneration. Beyond this threshold, Müller glial cells undergo structural remodeling and contribute to formation of subretinal glial membranes, reflecting a shift from homeostatic support to containment. This framework proposes a biologically testable staging axis from preserved Müller glial cell function to progressive dysfunction, aligning disease progression with therapeutic windows. Pre-ELM stages are characterized by retained plasticity and suitability for neuroprotective and metabolic interventions, whereas post-ELM stages require strategies focused on stabilization and limiting degeneration. Importantly, current clinical trials do not incorporate Müller glial cell state or ELM integrity as stratification variables, contributing to outcome insensitivity. In conclusion, Müller glial cells function as central regulators of retinal homeostasis and disease progression in AMD. Integrating glial biology with structural biomarkers may enable stage-specific precision therapies and improve clinical trial design.","PeriodicalId":21159,"journal":{"name":"Progress in Retinal and Eye Research","volume":"26 1","pages":""},"PeriodicalIF":17.8,"publicationDate":"2026-04-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147681455","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}

{"title":"Outer retinal tubulation associated with photoreceptor degeneration","authors":"Victor Lin ,&nbsp;Winston Lee ,&nbsp;Eugene Yu-Chuan Kang ,&nbsp;Pei-Kang Liu ,&nbsp;Nan-Kai Wang","doi":"10.1016/j.preteyeres.2026.101435","DOIUrl":"10.1016/j.preteyeres.2026.101435","url":null,"abstract":"<div><div>Outer retinal tubulation (ORT) is a distinct structural manifestation of chronic photoreceptor degeneration, observed across a broad spectrum of retinal diseases. Initially described histologically as rosette-like formations, ORT has gained clinical relevance with the advent of high-resolution imaging modalities such as spectral-domain optical coherence tomography (SD-OCT) and adaptive optics scanning laser ophthalmoscopy (AO-SLO), which enable <em>in vivo</em> visualization of its tubular architecture. ORT arises from sustained photoreceptor and retinal pigment epithelium (RPE) injury, leading to the reorganization of surviving cones ensheathed by gliotic Müller cell processes. This review integrates historical, histological, and imaging data to elucidate ORT's cellular composition, formation mechanisms, and disease-specific patterns. We introduce a novel etiological classification of ORT, categorized as degenerative, fibrotic, or edematous ORT according to predominant pathogenic drivers, to facilitate cross-disease comparison and prognostic stratification. Clinically, ORT serves as a non-exudative biomarker of chronic retinal injury, aiding differential diagnosis and informing treatment strategies. In age-related macular degeneration, ORT is associated with subretinal fibrosis and poor visual outcomes; in geographic atrophy, it may signal slower lesion progression. In inherited retinal dystrophies, ORT reflects genotype-specific vulnerabilities and residual photoreceptor survival, with implications for therapeutic targeting. As imaging technologies advance, ORT offers promise as a structural marker of disease chronicity, photoreceptor resilience, and Müller cell plasticity, enhancing diagnostic precision and supporting its role as a meaningful endpoint in clinical trials.</div></div>","PeriodicalId":21159,"journal":{"name":"Progress in Retinal and Eye Research","volume":"111 ","pages":"Article 101435"},"PeriodicalIF":14.7,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145995272","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}

{"title":"Structural photoreceptor evaluation in age-related macular degeneration. A comprehensive review of methods and clinical significance","authors":"Lourdes Vidal-Oliver ,&nbsp;Davide Garzone ,&nbsp;Lukas Schloesser ,&nbsp;Sarah Thiele ,&nbsp;Maximilian Pfau ,&nbsp;Wolf M. Harmening ,&nbsp;Julius Ameln ,&nbsp;Rosa Dolz-Marco ,&nbsp;Nicolas Cuenca ,&nbsp;Isabel Ortuño-Lizaran ,&nbsp;Zhichao Wu ,&nbsp;Robyn H. Guymer ,&nbsp;Robert P. Finger","doi":"10.1016/j.preteyeres.2026.101447","DOIUrl":"10.1016/j.preteyeres.2026.101447","url":null,"abstract":"<div><div>Age-related macular degeneration (AMD) is a disease that primarily affects the outer retina, with progressive photoreceptor degeneration and atrophy of the retinal pigment epithelium (RPE). Advances in imaging now enable photoreceptor changes to be detected and quantified with unprecedented sensitivity, whereas comparable biomarkers of RPE dysfunction remain less developed. As such, photoreceptor-based biomarkers are increasingly considered potential surrogates for current clinical trial endpoints. This review examines the current imaging modalities—particularly optical coherence tomography (OCT) and modalities enhanced by adaptive optics (AO) —used to evaluate photoreceptor structure in AMD. We explore the intrinsic value of parameters such as outer nuclear layer thickness, external limiting membrane integrity, photoreceptor inner and outer segment thickness, ellipsoid zone (EZ) integrity, and EZ reflectivity on OCT, and cone density and regularity on AO imaging, highlighting their potential and limitations. While OCT-based metrics are the most accessible in clinical settings, their clinical utility is hampered by inconsistent segmentation protocols and methodological heterogeneity. AO imaging offers unmatched resolution but faces practical barriers to widespread adoption. The field is moving in a promising direction with emerging computational tools and artificial intelligence improving accuracy and scalability. However, progress is contingent on establishing consensus definitions, standardized acquisition and analysis protocols, and normative datasets. Future efforts should focus on translating high-resolution imaging into robust, reproducible biomarkers that can be widely adopted in both clinical practice and therapeutic development.</div></div>","PeriodicalId":21159,"journal":{"name":"Progress in Retinal and Eye Research","volume":"111 ","pages":"Article 101447"},"PeriodicalIF":14.7,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146202568","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}

{"title":"Lens aging and disease: Molecular mechanisms, functional consequences, and pharmacological implications","authors":"Xingjun Fan ,&nbsp;Vincent M. Monnier","doi":"10.1016/j.preteyeres.2026.101446","DOIUrl":"10.1016/j.preteyeres.2026.101446","url":null,"abstract":"<div><div>Age-related cataract (ARC) remains the leading cause of blindness worldwide, reflecting the progressive failure of lifelong mechanisms that preserve the transparency and refractive precision of the ocular lens. The lens is uniquely vulnerable to aging because its core fiber cells, crystallin proteins, and lipids persist for decades without turnover, relying on stable protein solubility, redox homeostasis, membrane integrity, and tightly coordinated epithelial renewal. With age, gradual biochemical and biomechanical shifts, including crystallin oxidation and truncation, deamidation and racemization, glycation, formation of disulfide and non-disulfide crosslinks, membrane remodeling, and stiffening of the lens nucleus, erode the structural and optical properties required for clear vision. Decline in glutathione (GSH) synthesis and redox-repair enzymes amplifies oxidative damage, while emerging evidence identifies ferroptosis, rather than apoptosis, as a dominant regulated cell-death pathway compromising lens epithelial cell survival in aging. In parallel, genome-wide association studies and exome sequencing have revealed a complex polygenic architecture for ARC, highlighting modifier genes that influence cytoskeletal resilience, protein stability, ion transport, and systemic metabolic signaling. Environmental exposures, including ultraviolet radiation, smoking, heat stress, and air pollution, interact with these genetic and biochemical pathways to accelerate opacity formation. This review integrates recent advances in lens biology, proteomics, redox regulation, lipid and membrane biophysics, mechanobiology, and cell death signaling to provide a cohesive framework for understanding how age-related changes converge to produce cataract. We also outline emerging therapeutic strategies that target redox buffering, crystallin stability, epithelial survival pathways, and biomechanical properties of the aging lens.</div></div>","PeriodicalId":21159,"journal":{"name":"Progress in Retinal and Eye Research","volume":"111 ","pages":"Article 101446"},"PeriodicalIF":14.7,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146152643","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}

{"title":"Ocular gene therapy mediated by AAV vectors: an overview of immunosuppressive treatments and immunomonitoring of patients involved in clinical trials","authors":"Duohao Ren ,&nbsp;Gaelle A. Chauveau ,&nbsp;Emilie Cabon ,&nbsp;Julie Vendomèle ,&nbsp;Catherine Vignal-Clermont ,&nbsp;Hanadi Saliba ,&nbsp;Divya Ail ,&nbsp;Deniz Dalkara ,&nbsp;Sylvain Fisson","doi":"10.1016/j.preteyeres.2026.101443","DOIUrl":"10.1016/j.preteyeres.2026.101443","url":null,"abstract":"<div><div>Hereditary retinal diseases (RDs) are a group of diseases caused by monogenetic or multigenetic mutations in genes mostly expressed in the photoreceptors. RDs can eventually lead to severe vision impairment or blindness. Since the 1990s, ocular gene transfer mediated by adeno-associated virus (AAV)-derived vectors has been explored to treat hereditary ocular diseases via gene supplementation or gene editing, advancing gene therapy to the clinical trial stages and to one commercial product. By the end of 2024, 142 clinical trials had been initiated for different types of RDs. Immune responses remain a major concern in AAV-mediated gene therapy. Although the eye is considered as an immune-privileged organ, studies in animals and clinical evidence have demonstrated that ocular gene therapies mediated by AAV can trigger immune responses to the vector capsid and/or to the transgene genome and product. These immune responses may compromise the efficiency and safety of the therapy. In this review, we summarize clinical trials treating RDs with AAV and provide a comprehensive overview of reported immune responses, including local inflammation and systemic adaptive immune responses. Additionally, this review emphasizes that immunosuppression and immunomonitoring strategies are not yet standardized both for intraocular and systemic gene therapy clinical trials, and do not allow for accurate follow-up of side effects. It highlights the inter-individual variability among patients, reinforcing the need to evaluate multiple key immune parameters, including sensitive inflammation biomarkers, and to assess the impact of different immunosuppression regimens.</div></div>","PeriodicalId":21159,"journal":{"name":"Progress in Retinal and Eye Research","volume":"111 ","pages":"Article 101443"},"PeriodicalIF":14.7,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146089552","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}

{"title":"Age-related macular degeneration and cerebral amyloid angiopathy have similar pathologies from cholesterol-APOE-amyloid-β-complement mediated inflammation","authors":"Whitney Stuard Sambhariya ,&nbsp;Catherine Bowes Rickman ,&nbsp;Patricia A. D'Amore ,&nbsp;Giulia Corradetti ,&nbsp;Gregory S. Hageman ,&nbsp;Gareth R. Howell ,&nbsp;Olivia J. Marola ,&nbsp;Hemali Phatnani ,&nbsp;Nancy J. Philp ,&nbsp;Debasish Sinha ,&nbsp;Christopher B. Toomey ,&nbsp;Faith Stone ,&nbsp;Charles Eberhart ,&nbsp;James T. Handa","doi":"10.1016/j.preteyeres.2026.101449","DOIUrl":"10.1016/j.preteyeres.2026.101449","url":null,"abstract":"<div><div>Age-related macular degeneration (AMD) and Alzheimer's disease (AD) are neurodegenerative conditions that afflict millions of elderly people around the world. AMD is a progressive retinal disorder that leads to central vision loss whereas AD primarily causes cognitive decline and behavioral changes. While each disease has distinct clinical manifestations, the accumulation of extracellular amyloid-β is a common histopathologic finding. Similarly, cerebral amyloid angiopathy (CAA), a vascular condition that can exist independent or with AD, is characterized by the accumulation of amyloid-β in cerebral blood vessels. While significant investigation of the pathophysiologic links between AMD and AD has been conducted, the underlying similarities and differences in the pathobiology of AMD and CAA has not been considered. In this review, we discuss the common pathological features of these two conditions. We then discuss the similar pathobiology that involves cholesterol metabolism, apolipoprotein E, amyloid-β, and complement mediated inflammation. At the same time, we discuss key differences in their pathobiology. This discussion sheds new perspective and insights of their pathobiology.</div></div>","PeriodicalId":21159,"journal":{"name":"Progress in Retinal and Eye Research","volume":"111 ","pages":"Article 101449"},"PeriodicalIF":14.7,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146208854","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}

{"title":"Epigenetic reprogramming for ocular aging and disease: Mechanisms, biomarkers, and the road to the clinic","authors":"Junwon Lee ,&nbsp;Minseok Han ,&nbsp;Kaixiang Wang ,&nbsp;L. Rainer Butler ,&nbsp;David A. Sinclair","doi":"10.1016/j.preteyeres.2026.101442","DOIUrl":"10.1016/j.preteyeres.2026.101442","url":null,"abstract":"<div><div>The eye's visual function relies on retinal neural cells that are long-lived, post-mitotic, and possess minimal regenerative capacity. These combined properties render them exceptionally vulnerable to the cumulative damage that drives age-related functional decline. Accumulating evidence now implicates epigenetic alterations, such as aberrant DNA methylation and histone modifications, not merely as correlates of aging but as fundamental drivers of aging and disease. These changes disrupt the stable gene expression programs required to maintain cellular identity and function, thereby contributing to the pathogenesis of irreversible blinding diseases like glaucoma and age-related macular degeneration (AMD). Unlike immutable genetic mutations, the reversible nature of these epigenetic marks offers a novel therapeutic paradigm. Epigenetic reprogramming, a strategy involving the transient expression of Yamanaka factors or chemical cocktails, provides a powerful means to reset this dysregulated epigenetic landscape and restore cells to a more youthful state. Compelling preclinical studies have validated this approach by demonstrating vision restoration in models of optic neuropathy through the rejuvenation of damaged and aged neurons. This review provides a comprehensive overview of ocular aging from an epigenetic perspective, examines the promise and potential concerns of epigenetic reprogramming, and discusses the future of rejuvenation therapies in ophthalmology.</div></div>","PeriodicalId":21159,"journal":{"name":"Progress in Retinal and Eye Research","volume":"111 ","pages":"Article 101442"},"PeriodicalIF":14.7,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146032817","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}

{"title":"Vogt-Koyanagi-Harada disease under the lens: Insights from multimodal ocular imaging","authors":"Lan Xia ,&nbsp;Ling Chen ,&nbsp;Lingyu Dai ,&nbsp;Pei Zhang ,&nbsp;Carlos Cifuentes-González ,&nbsp;Vishali Gupta ,&nbsp;Rupesh Agrawal ,&nbsp;Peizeng Yang","doi":"10.1016/j.preteyeres.2026.101445","DOIUrl":"10.1016/j.preteyeres.2026.101445","url":null,"abstract":"<div><div>Vogt-Koyanagi-Harada (VKH) disease is a multisystem autoimmune condition targeting melanocyte-rich ocular tissues, with inflammation primarily affecting the choroid. Despite advances in diagnostic criteria, disease staging and therapeutic decisions still rely heavily on clinical observation, with limited integration of imaging biomarkers. This review examines the evolving role of multimodal ocular imaging (MMI) in the diagnosis, monitoring, and prognostication of VKH.</div><div>We critically appraise the utility and limitations of color fundus photography, fluorescein angiography (FFA), indocyanine green angiography (ICGA), optical coherence tomography (OCT), OCT angiography (OCTA), fundus autofluorescence, B-scan ultrasonography, ultrasound biomicroscopy and anterior segment photography. These modalities provide complementary insights into disease activity, from subclinical choroiditis and retinal pigment epithelium disruption to chronic sequelae such as subretinal fibrosis and choroidal atrophy. Key imaging features—such as choroidal thickening, hypofluorescent dark dots, RPE undulations, and flow voids—are described in the context of VKH pathophysiology and disease stage.</div><div>We identify critical gaps in current practice, including the lack of standardized imaging-based definitions for relapse and remission, limited use of anterior segment imaging, and variability in access to advanced modalities. To address these challenges, we propose a stage-specific imaging framework to guide VKH assessment from prodromal to chronic phases.</div><div>MMI has transitioned from a supportive to a central role in VKH management. Future efforts should prioritize the development of quantitative imaging biomarkers, standardization of grading systems, and integration of imaging into therapeutic algorithms to support timely, personalized care and prevent irreversible visual loss.</div></div>","PeriodicalId":21159,"journal":{"name":"Progress in Retinal and Eye Research","volume":"111 ","pages":"Article 101445"},"PeriodicalIF":14.7,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146126191","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}