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Vogt-Koyanagi-Harada Disease Under the Lens: Insights from Multimodal Ocular Imaging. 镜头下的Vogt-Koyanagi-Harada病:来自多模态眼成像的见解。
IF 14.7 1区 医学 Q1 OPHTHALMOLOGY Pub Date : 2026-02-04 DOI: 10.1016/j.preteyeres.2026.101445
Lan Xia, Ling Chen, Lingyu Dai, Pei Zhang, Carlos Cifuentes-González, Vishali Gupta, Rupesh Agrawal, Peizeng Yang

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. 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. 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. 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.

Vogt-Koyanagi-Harada (VKH)病是一种针对富含黑素细胞的眼部组织的多系统自身免疫性疾病,炎症主要影响脉络膜。尽管诊断标准有所进步,但疾病分期和治疗决策仍然严重依赖临床观察,影像生物标志物的整合有限。本文综述了多模态眼成像(MMI)在VKH的诊断、监测和预测中的作用。我们批判性地评估彩色眼底摄影、荧光素血管造影(FFA)、吲哚菁绿血管造影(ICGA)、光学相干断层扫描(OCT)、OCT血管造影(OCTA)、眼底自体荧光、b超、超声生物显微镜和前段摄影的实用性和局限性。这些模式提供了对疾病活动的补充见解,从亚临床脉络膜炎和视网膜色素上皮破坏到慢性后遗症,如视网膜下纤维化和脉络膜萎缩。关键的影像学特征,如脉络膜增厚、低荧光黑点、RPE波动和流动空洞,在VKH病理生理和疾病分期的背景下被描述。我们确定了当前实践中的关键差距,包括缺乏基于复发和缓解的标准化成像定义,前节段成像的使用有限,以及获得高级模式的可变性。为了应对这些挑战,我们提出了一个特定阶段的成像框架,以指导从前驱期到慢性期的VKH评估。MMI已经从VKH管理的支持角色转变为核心角色。未来的努力应优先发展定量成像生物标志物,标准化分级系统,并将成像整合到治疗算法中,以支持及时,个性化的护理和防止不可逆转的视力丧失。
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引用次数: 0
Ocular gene therapy mediated by AAV vectors: an overview of immunosuppressive treatments and immunomonitoring of patients involved in clinical trials AAV载体介导的眼部基因治疗:免疫抑制治疗和临床试验患者免疫监测综述
IF 17.8 1区 医学 Q1 OPHTHALMOLOGY Pub Date : 2026-01-30 DOI: 10.1016/j.preteyeres.2026.101443
Duohao Ren, Gaelle A. Chauveau, Emilie Cabon, Julie Vendomèle, Catherine Vignal-Clermont, Hanadi Saliba, Divya Ail, Deniz Dalkara, Sylvain Fisson
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引用次数: 0
Epigenetic reprogramming for ocular aging and disease: Mechanisms, biomarkers, and the road to the clinic 眼老化和疾病的表观遗传重编程:机制、生物标志物和临床之路
IF 14.7 1区 医学 Q1 OPHTHALMOLOGY Pub Date : 2026-01-21 DOI: 10.1016/j.preteyeres.2026.101442
Junwon Lee , Minseok Han , Kaixiang Wang , L. Rainer Butler , David A. Sinclair
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.
眼睛的视觉功能依赖于视网膜神经细胞,这些细胞是长寿命的,有丝分裂后的,并且具有最小的再生能力。这些综合特性使它们特别容易受到累积损伤,从而导致与年龄相关的功能衰退。越来越多的证据表明,表观遗传改变,如异常的DNA甲基化和组蛋白修饰,不仅是衰老的相关因素,而且是衰老和疾病的基本驱动因素。这些变化破坏了维持细胞身份和功能所需的稳定基因表达程序,从而导致了青光眼和年龄相关性黄斑变性(AMD)等不可逆致盲疾病的发病机制。与不可变的基因突变不同,这些表观遗传标记的可逆性提供了一种新的治疗范式。表观遗传重编程是一种涉及山中因子或化学混合物的短暂表达的策略,它提供了一种强大的手段来重置这种失调的表观遗传景观,使细胞恢复到更年轻的状态。令人信服的临床前研究证实了这种方法,通过损伤和老化神经元的再生,在视神经病变模型中证明了视力恢复。本文从表观遗传学的角度对眼老化进行了全面的综述,探讨了表观遗传重编程的前景和潜在的问题,并讨论了眼科年轻化治疗的未来。
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引用次数: 0
Aging, oxidative stress, and cataracts: Therapeutic prospects and translational insights into peroxiredoxin 6 衰老,氧化应激和白内障:治疗前景和对过氧化物还氧蛋白6的翻译见解
IF 14.7 1区 医学 Q1 OPHTHALMOLOGY Pub Date : 2026-01-21 DOI: 10.1016/j.preteyeres.2026.101444
Eri Kubo , Bhavana Chhunchha , Dhirendra P. Singh
Selenium-independent peroxiredoxin 6 (Prdx6) is a unique member of the peroxiredoxin family, which protects cells from various stressors by regulating reactive oxygen species (ROS) and maintaining survival signaling. As a multifunctional "moonlighting" protein, Prdx6 exhibits glutathione peroxidase (GPx), acidic calcium-independent phospholipase A2, and lysophosphatidylcholine acyltransferase activities, enabling it to reduce ROS. Loss of Prdx6, owing to dysregulation of its transactivator nuclear factor erythroid 2-related factor 2 or aberrant oxidative post-translational modifications from aging or oxidative stress, disrupts cellular homeostasis and triggers inflammatory or non-inflammatory cell death, including apoptosis and pyroptosis. Similar to GPx4, Prdx6 exhibits selenium-independent peroxidase activity and possesses phospholipid hydroperoxide–reducing GPx activity. A novel function of Prdx6 in facilitating selenium utilization was identified recently; that is, it enhances the expression and activity of selenoproteins, especially GPx4, and prevents ferroptosis. Conversely, Prdx6 deficiency reduces selenoprotein levels and promotes ferroptosis. Nevertheless, the molecular mechanisms through which Prdx6 modulates cell death and survival, particularly under aging and oxidative stress conditions contributing to cataractogenesis, remain unclear. In this review, we summarize the current knowledge of Prdx6 regulation and activity during oxidative stress and aging, highlighting its role in inflammatory and non-inflammatory signaling that contributes to eye lens pathology and cataract formation. Additionally, we discuss natural activators and potential therapeutic strategies targeting Prdx6 to extend eye lens health and delay or prevent cataract development. Overall, we conclude that enhancing Prdx6 activity offers a promising strategy to prevent or reverse age-related cataracts.
硒独立过氧化物还蛋白6 (Prdx6)是过氧化物还蛋白家族的独特成员,通过调节活性氧(ROS)和维持生存信号来保护细胞免受各种应激源的影响。作为一种多功能的“兼职”蛋白,Prdx6具有谷胱甘肽过氧化物酶(GPx)、酸性钙非依赖性磷脂酶A2和溶血磷脂酰转移酶活性,使其能够减少ROS。Prdx6的缺失,由于其反激活因子核因子红系2相关因子2的失调或老化或氧化应激引起的异常氧化翻译后修饰,破坏细胞稳态并引发炎症或非炎症性细胞死亡,包括凋亡和焦亡。与GPx4类似,Prdx6具有硒不依赖性过氧化物酶活性,并具有磷脂氢过氧化物还原GPx活性。最近发现了Prdx6在促进硒利用方面的新功能;即增强硒蛋白,尤其是GPx4的表达和活性,防止铁下垂。相反,Prdx6缺乏降低硒蛋白水平,促进铁下垂。然而,Prdx6调节细胞死亡和存活的分子机制,特别是在衰老和氧化应激条件下导致白内障发生的机制尚不清楚。在这篇综述中,我们总结了Prdx6在氧化应激和衰老过程中的调节和活性的现有知识,强调了它在炎症和非炎症信号传导中的作用,这些信号传导有助于晶状体病理和白内障的形成。此外,我们还讨论了针对Prdx6的天然激活剂和潜在的治疗策略,以延长眼晶状体健康,延缓或预防白内障的发展。总之,我们得出结论,增强Prdx6活性为预防或逆转年龄相关性白内障提供了一个有希望的策略。
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引用次数: 0
Outer retinal tubulation associated with photoreceptor degeneration 视网膜外管化与光感受器变性有关
IF 14.7 1区 医学 Q1 OPHTHALMOLOGY Pub Date : 2026-01-16 DOI: 10.1016/j.preteyeres.2026.101435
Victor Lin , Winston Lee , Eugene Yu-Chuan Kang , Pei-Kang Liu , Nan-Kai Wang
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 in vivo 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.
视网膜外管化(ORT)是慢性光感受器变性的一种独特的结构表现,在广泛的视网膜疾病中观察到。ORT最初在组织学上被描述为玫瑰状结构,随着高分辨率成像方式的出现,如光谱域光学相干断层扫描(SD-OCT)和自适应光学扫描激光检眼镜(AO-SLO)的出现,ORT获得了临床意义,这些成像方式能够在体内可视化其管状结构。ORT是由持续的光感受器和视网膜色素上皮(RPE)损伤引起的,导致被胶质细胞勒细胞突包裹的幸存视锥细胞重组。这篇综述整合了历史、组织学和影像学数据来阐明ORT的细胞组成、形成机制和疾病特异性模式。我们介绍了一种新的ORT病因学分类,根据主要的致病因素将ORT分类为退行性、纤维化性或水肿性,以便于跨疾病比较和预后分层。在临床上,ORT作为慢性视网膜损伤的非渗出性生物标志物,有助于鉴别诊断和指导治疗策略。在年龄相关性黄斑变性中,ORT与视网膜下纤维化和视力不良有关;在地理萎缩中,它可能表明病变进展较慢。在遗传性视网膜营养不良症中,ORT反映了基因型特异性脆弱性和残留的光感受器存活,具有治疗靶向性。随着成像技术的进步,ORT有望作为疾病慢性、光感受器恢复力和勒细胞可塑性的结构标记物,提高诊断精度,并支持其作为临床试验中有意义的终点的作用。
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引用次数: 0
Surgical management of myopic traction maculopathy; expert perspectives from the myopia society 近视牵引性黄斑病变的外科治疗近视学会专家的观点
IF 14.7 1区 医学 Q1 OPHTHALMOLOGY Pub Date : 2026-01-01 DOI: 10.1016/j.preteyeres.2025.101434
Hiroyuki Takahashi , Richard F. Spaide , Shu Yen Lee , Yasushi Ikuno , Pei-Ting Lu , Chi-Chun Lai , Yuxin Fang , Chui Ming Gemmy Cheung , Jose M. Ruiz-Moreno , Kyoko Ohno-Matsui
Myopic traction maculopathy (MTM) occurs in approximately 9–34 % of highly myopic eyes and requires surgical treatment to prevent irreversible vision loss due to progression to macular hole (MH) or retinal detachment (RD). While treatment of MTM, which presents with a variety of morphological patterns, shares the common goal of managing the causative tractional tissues on the retina, it is essential to tailor the surgical plan according to the locations of each lesion. Here, we classify MTM into four core lesions: retinoschisis, foveal RD, lamellar MH (LMH), and full-thickness MH (FTMH), and present an algorithm for treatment decision-making. Pars plana vitrectomy (PPV) is a procedure that enables reliable removal of traction-inducing tissues and should be promptly indicated for patients with foveal RD showing progressive vision decline or those with MHRD. Postoperatively, development of macular hole or progression of macular atrophy should be monitored carefully. In recurrent MTM, inadequate membrane peeling is a common cause, requiring wide-field imaging and more intensive intraoperative assessment for residual tissues. Recurrent MTM without FTMH is treated with additional ILM peeling, while recurrence with FTMH is managed surgically using techniques involving ILM flaps, autologous retinal flap, or amniotic membrane transplantation. Macular buckling has also been reported to be effective when used alone or in combination with PPV. Following treatment, long-term follow-up is essential for monitoring both recovery and recurrence. Though further validation through randomized prospective trials is needed, the paradigm for MTM surgery continues to evolve toward preventing persistent vision loss and to optimizing long-term outcomes.
近视牵引力黄斑病变(MTM)发生在大约9 - 34%的高度近视眼睛中,需要手术治疗以防止由于黄斑孔(MH)或视网膜脱离(RD)的进展而导致的不可逆视力丧失。MTM具有多种形态模式,治疗MTM的共同目标是控制视网膜上的致病牵引组织,根据每个病变的位置定制手术计划是至关重要的。在这里,我们将MTM分为四种核心病变:视网膜裂、中央凹RD、板层MH (LMH)和全层MH (FTMH),并提出了一种治疗决策算法。玻璃体切割(PPV)是一种能够可靠地切除牵拉诱导组织的手术,对于出现进行性视力下降的中央凹RD患者或MHRD患者应及时进行手术。术后应仔细观察黄斑裂孔的发展或黄斑萎缩的进展。在复发性MTM中,膜剥离不充分是常见的原因,需要宽视场成像和术中对残余组织进行更深入的评估。复发性MTM无FTMH的治疗采用额外的ILM剥离,而复发的FTMH则采用包括ILM瓣、自体视网膜瓣或羊膜移植在内的手术技术。黄斑屈曲单独使用或与PPV联合使用也有报道。治疗后,长期随访是监测恢复和复发的必要条件。虽然需要通过随机前瞻性试验进一步验证,但MTM手术的范例继续朝着预防持续性视力丧失和优化长期结果的方向发展。
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引用次数: 0
Glymphatic transport and ocular diseases 淋巴转运与眼部疾病
IF 14.7 1区 医学 Q1 OPHTHALMOLOGY Pub Date : 2026-01-01 DOI: 10.1016/j.preteyeres.2025.101433
Xiaowei Wang , Christine Delle , Maiken Nedergaard , Peter Wostyn
The high metabolic demand of retinal neurons requires tightly regulated mechanisms to maintain homeostasis and ensure the efficient clearance of metabolic waste and excess water. Recent studies have identified a glymphatic-like system in the rodent eye, and growing evidence supports the existence of a similar pathway in the human eye, facilitating fluid exchange and waste removal. The ocular glymphatic system supports bidirectional flow along the optic nerve - anterograde from the retina and retrograde from the brain.
In this review, we integrate findings from preclinical models and clinically grounded hypotheses to identify key contributors to glymphatic dysfunction in ocular diseases. These include impaired laminar barrier integrity, pathological perivascular space expansion, aquaporin-4 abnormalities, immature vasculature, and pathological immune activation. Glymphatic impairment has been implicated in murine models of glaucoma, diabetic retinopathy, and ocular manifestations of Alzheimer's disease. Additionally, disrupted glymphatic flow is suspected in papilledema, spaceflight associated neuro-ocular syndrome, and Terson syndrome.
We further explore novel associations between glymphatic dysfunction and other blinding disorders such as myopic optic neuropathy, age-related macular degeneration, neuromyelitis optica spectrum disorders, and retinal vasculitis. In delineating these mechanistic links, this review provides a conceptual framework to guide future research in glymphatic contributions to ocular diseases.
视网膜神经元的高代谢需求需要严格调节机制来维持体内平衡,并确保代谢废物和多余水分的有效清除。最近的研究已经在啮齿动物的眼睛中发现了一个类淋巴系统,并且越来越多的证据支持在人眼中存在类似的途径,促进液体交换和废物清除。眼淋巴系统支持沿视神经的双向流动——视网膜的顺行和大脑的逆行。在这篇综述中,我们整合了临床前模型和临床假设的发现,以确定眼病中淋巴功能障碍的关键因素。这些包括层膜屏障完整性受损、病理性血管周围空间扩张、水通道蛋白-4异常、血管不成熟和病理性免疫激活。在青光眼、糖尿病视网膜病变和阿尔茨海默病的眼部表现的小鼠模型中,已经发现了淋巴细胞损伤。此外,在乳头水肿、航天相关的神经-眼综合征和Terson综合征中,怀疑淋巴血流紊乱。我们进一步探讨了淋巴功能障碍与其他致盲疾病(如近视视神经病变、年龄相关性黄斑变性、视神经脊髓炎和视网膜血管炎)之间的新联系。在描述这些机制联系的过程中,本综述提供了一个概念框架,以指导未来关于淋巴细胞在眼部疾病中的作用的研究。
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引用次数: 0
Mitochondria in corneal physiology and pathology: A mechanistic perspective 线粒体在角膜的生理和病理:一个机制的观点
IF 14.7 1区 医学 Q1 OPHTHALMOLOGY Pub Date : 2026-01-01 DOI: 10.1016/j.preteyeres.2025.101432
Liusi Yang , Siyi Chen , Jiayun Ge , Zhitong Chen , Kuangqi Chen , Jiahui Li , Jiaxin Zhang , Ya Li , Mingli Qu , Dawn J.H. Neo , Xuhong Zhang , Xiang Li , Yinhao Wang , Qianjie Yang , Xiangzheng Zhang , Dongjie Song , Xiuyi Li , Lin Du , Ye Shen , Weiyun Shi , Jianping Tong
The cornea is the eye's outermost protective and refractive barrier whose physiological homeostasis depends on mitochondrial competence and dynamic stability. Mitochondrial dysfunctions are characterized by impaired electron transport chain efficiency, excessive reactive oxygen species generation, calcium dysregulation, and disrupted dynamics. Clinically, mitochondrial dysfunctions underlie the pathogenesis of diverse corneal disorders, including Fuchs endothelial corneal dystrophy, dry eye disease, diabetic keratopathy, keratoconus and infectious keratitis. Although prior work has linked mitochondrial dysfunction to corneal pathology, an integrated, mechanism-to-therapy synthesis remains limited. Dysregulated mitochondrial redox signaling exacerbates oxidative stress and the release of mitochondrial-derived damage-associated molecular patterns, triggering inflammatory cascades and cell death pathways. Imbalances in mitochondrial metabolism and dynamics further amplify cellular damage and disease progression. This review systematically delineates mitochondria's roles in corneal energy supply and homeostatic regulation, clarifies the causal involvement of mitochondrial dysfunction and dysregulated networks in corneal disease pathogenesis. More importantly, by elucidating the intricate mechanisms of mitochondrial regulation and dysfunction, this review underscores the transformative potential of mitochondria-targeted interventions in advancing corneal disease management and improving clinical outcome.
角膜是眼睛最外层的保护和屈光屏障,其生理稳态取决于线粒体能力和动态稳定性。线粒体功能障碍的特征是电子传递链效率受损、活性氧产生过多、钙调节失调和动力学破坏。临床上,线粒体功能障碍是多种角膜疾病的发病机制基础,包括Fuchs内皮性角膜营养不良、干眼病、糖尿病性角膜病变、圆锥角膜和感染性角膜炎。尽管先前的研究已将线粒体功能障碍与角膜病理联系起来,但综合的机制-治疗综合仍然有限。线粒体氧化还原信号失调加剧了氧化应激和线粒体衍生的损伤相关分子模式的释放,引发炎症级联反应和细胞死亡途径。线粒体代谢和动力学的不平衡进一步放大了细胞损伤和疾病进展。本文系统地阐述了线粒体在角膜能量供应和稳态调节中的作用,阐明了线粒体功能障碍和失调网络在角膜疾病发病机制中的因果关系。更重要的是,通过阐明线粒体调控和功能障碍的复杂机制,本综述强调了线粒体靶向干预在推进角膜疾病管理和改善临床结果方面的变革潜力。
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引用次数: 0
Femtosecond lasers in ophthalmology: Mechanisms, clinical breakthroughs, and multidisciplinary frontiers 飞秒激光在眼科:机制、临床突破和多学科前沿
IF 14.7 1区 医学 Q1 OPHTHALMOLOGY Pub Date : 2025-12-06 DOI: 10.1016/j.preteyeres.2025.101431
Wan-Ping Zhang , Hai-Jun Lv , An-Peng Pan , Wan-Xia Zhang , Xu Shao , Yong-Zheng Qu , An-Song Li , Lin-Hua Chen , Shao-Qun Zeng , A-Yong Yu
Femtosecond laser (FSL) technology has emerged as a transformative force in ophthalmology, offering unprecedented precision in tissue manipulation with minimal collateral thermal and mechanical damage. This comprehensive review traces the evolution of FSL from its fundamental physical principles to its broad spectrum of clinical applications. We examine its roles in refractive surgery, corneal transplantation, presbyopia correction, cataract surgery, glaucoma management, and pterygium excision, as well as recent advancements in intraocular lens customization and nanopatterning. Beyond established clinical use, we explore emerging frontiers where FSL intersects with optogenetics, two-photon photodynamic therapy, and artificial intelligence-augmented optical coherence tomography. Unresolved challenges, including reactive oxygen species-mediated toxicity, cost limitations, and long-term biosafety, are critically discussed. By integrating mechanistic insights, clinical evidence, and translational prospects, this review highlights the potential of FSL to redefine ophthalmic practice through interdisciplinary innovation and to enable the development of personalized, minimally invasive therapeutic strategies.
飞秒激光(FSL)技术已经成为眼科的变革力量,在组织操作方面提供前所未有的精度,同时最小的附带热损伤和机械损伤。这篇全面的综述追溯了FSL从其基本物理原理到广泛临床应用的演变。我们研究了它在屈光手术、角膜移植、老花眼矫正、白内障手术、青光眼治疗和翼状胬肉切除中的作用,以及人工晶状体定制和纳米模式的最新进展。除了既定的临床应用之外,我们还探索了FSL与光遗传学、双光子光动力疗法和人工智能增强光学相干断层扫描交叉的新兴领域。尚未解决的挑战,包括活性氧物种介导的毒性,成本限制和长期生物安全性,进行了批判性的讨论。通过整合机制见解、临床证据和转化前景,本综述强调了FSL通过跨学科创新重新定义眼科实践的潜力,并使个性化、微创治疗策略的发展成为可能。
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引用次数: 0
Beyond convolutions and supervised learning with transformers and representation learning for retinal image analysis 超越卷积和监督学习与变压器和表示学习视网膜图像分析
IF 14.7 1区 医学 Q1 OPHTHALMOLOGY Pub Date : 2025-12-04 DOI: 10.1016/j.preteyeres.2025.101419
Yue Wu , Cecilia S. Lee , Aaron Y. Lee
Retinal image analysis has enjoyed groundbreaking advances in the last ten years due to seismic improvements in image analysis techniques from the field of computer vision. Previous reviews in deep learning and artificial intelligence (AI) (Schmidt-Erfurth et al., 2018; Ting et al., 2019) have either focused on supervised learning, where labels are curated or manually created, or concentrated on the application of AI in specific image modalities and retina diseases (Hormel et al., 2021; Li et al., 2024a (Hormel et al., 2021, Li et al., 2024a)). In this review, we sought to summarize the advances in the field with the shift towards label-free approaches using representational learning and the emergence of vision transformers as alternatives to convolutional neural networks for image analysis. These advances include semi-supervised learning, self-supervised learning and directly led to the advent of foundation models, vision-language models, and multi-modal models.
由于计算机视觉领域的图像分析技术的巨大改进,视网膜图像分析在过去十年中取得了突破性的进展。之前关于深度学习和人工智能(AI)的综述[(Schmidt-Erfurth et al. 2018), (Ting et al. 2019)]要么专注于监督学习,其中标签是精心设计或手动创建的,要么专注于AI在特定图像模式和视网膜疾病中的应用[(Hormel et al. 2021), (Li et al. 2021)。[2024a] (Hormel et al., 2021; Li et al., 2024a)。在这篇综述中,我们试图总结该领域的进展,包括使用表征学习向无标签方法的转变,以及视觉转换器作为图像分析卷积神经网络的替代品的出现。这些进步包括半监督学习、自监督学习,并直接导致了基础模型、视觉语言模型和多模态模型的出现。
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引用次数: 0
期刊
Progress in Retinal and Eye Research
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