青光眼是一组以视盘萎缩凹陷、视野缺损以及视力下降为共同特征的视神经退行性疾病，也是世界首位不可逆性致盲眼病，导致患者生活质量降低、引起极大卫生经济负担。但其发病机制尚不明确，促进房水排出从而降低眼内压仍是目前减缓疾病进展的唯一治疗手段。房水排出的主要途径是经由小梁网进入Schlemm's管最后汇入巩膜外静脉，因此小梁网在调节房水排出以及平衡眼内压方面发挥重要作用。近年来，体内以及体外房水排出测量技术和小梁网成像技术不断突破，众多研究表明小梁网存在压力依赖的节律性搏动，在房水的脉冲式排出中起到关键作用，但在青光眼中这种搏动随疾病的进展减弱甚至消失。文章以小梁网的泵理论为核心，总结青光眼中房水排出的最新研究进展，并从恢复小梁网功能的角度出发探索可能有效的治疗策略，为青光眼的临床诊治提供新的思路。

Glaucoma, a group of optic nerve degenerative diseases, is characterized by papillary atrophy, visual field defects, and decreased vision. It is also the leading cause of irreversible blindness worldwide, significantly reducing patients’ the quality of life of patients and posing considerable health economic burdens. However, the pathogenesis of glaucoma remains unclear, and promoting aqueous humor outflow to reduce intraocular pressure is the only treatment option available to slow disease progression. The main pathway for aqueous humor outflow is through the trabecular meshwork into Schlemm's canal and finally into the episcleral veins, highlighting the crucial role of the trabecular meshwork in regulating aqueous humor outflow and maintaining intraocular pressure balance. In recent years, there have been notable breakthroughs in in vivo and in vitro aqueous humor outflow measurement techniques and trabecular meshwork imaging technologies.Many studies suggest that the trabecular meshwork exhibits pressure-dependent rhythmic pulsation, playing a crucial role in the pulse-like outflow of aqueous humor. Unfortunately, in glaucoma, this pulsation weakens or even disappears as the disease progresses. This article focuses on the trabecular meshwork's pump theory and summarizes the latest research progress in aqueous humor outflow in glaucoma, exploring potential effective therapeutic strategies aimed at restoring trabecular meshwork function. This provides new insights for the clinical diagnosis and treatment of glaucoma.

青光眼是全球第一大不可逆性致盲性眼病，影响全球7 000多万人，其特征是视网膜神经节细胞的退行性病变。到2040年，预计全球青光眼患者人数将增加至1.12亿，其中约10%的人至少一只眼睛失明。由高眼压诱发、多种致病因素导致的视网膜神经节细胞死亡是青光眼进展过程中视功能损伤的主要病理过程，也是青光眼病程中视功能损害不可逆的重要原因。目前降眼压治疗是唯一的干预疗法，然而其仍然不能完全遏止视网膜神经节细胞进行性损伤，并且既往病程造成的视神经损伤不可逆转。探索青光眼进程中视网膜神经节细胞退行性改变的直接致病因素，寻找关键的治疗靶点，以及开发新的具有神经保护作用的治疗药物，具有重要意义。文章回顾了近年来青光眼中视网膜神经节细胞退行性病变的机制和治疗的新进展，强调了神经血管单元的改变在青光眼发病机制中的重要作用和干预价值。同时，靶向代谢的药物应用、抑制早期炎症反应和减少氧化应激，辅以营养和运动支持等可能延缓和抑制神经退行性病变的发生，起到神经保护作用。未来青光眼发病机制的研究重点仍然在眼压之外的致病因素上，从血流、代谢和免疫串扰的病理环境中发掘对神经退行性改变重要的致病因素并进行干预治疗具有广阔的前景。在多种动物模型中验证干预手段的神经保护作用，也有望提高青光眼神经保护的临床转化成功率，以拓展青光眼的治疗理念与药物选择。

Glaucoma stands as the leading cause of irreversible blindness globally, affecting over 70 million individuals. It is characterized by progressive degeneration of retinal ganglion cells (RGCs). By 2040, the global prevalence of glaucoma is expected to rise to 112 million, with approximately 10% experiencing blindness in at least one eye. The primary pathological basis for visual function impairment in glaucoma progression is the loss of RGCs induced by elevated intraocular pressure (IOP) and various pathogenic factors. Currently, IOP-lowering treatment is the only intervention available, but it cannot completely halt the progressive injury to RGCs, nor can it reverse the optic nerve damage caused by prior disease progression. Exploring the direct pathogenic factors of RGC degeneration in glaucoma, identifying key therapeutic targets, and developing new neuroprotective treatments are of great importance. This review discusses recent advancements in the mechanisms and treatments of retinal ganglion cell degeneration in glaucoma, highlighting the significant role of neurovascular unit changes in the pathogenesis of glaucoma and the potential value of interventions. Additionally, targeting metabolites, inhibiting early inflammatory responses, and reducing oxidative stress, supplemented by nutritional and exercise support, may help delay and inhibit neurodegenerative processes, offering neuroprotective effects.Future research on glaucoma pathogenesis should focus on factors beyond IOP, exploring pathogenic factors in the pathological environment of blood flow, metabolism, and immune crosstalk for targeted therapeutic interventions. Also, verifying the neuroprotective effects of these interventions in various animal models holds promise for improving the clinical translation success rate of neuroprotection in glaucoma, thus expanding therapeutic concepts and drug options.

越来越多的证据表明，空气污染可严重损害人体健康，成为全球疾病负担的主要原因。并且污染空气中的主要成分空气颗粒物可渗透到肺部和心血管系统，引起缺血性心脏病、肺炎、慢性阻塞性肺疾病甚至肺癌，导致空气污染相关的发病率和死亡率升高。城市颗粒物作为城市居住人群面临的主要空气污染问题，被证实与多种炎症性眼表疾病密切相关，如过敏性结膜炎、角膜炎、干眼等。高浓度城市颗粒物暴露还会引起睑板腺病理性结构改变和功能异常，诱发炎性睑板腺功能障碍。文章综述了城市颗粒物相关的眼表疾病类型及其致病机制的最新研究，旨在阐明空气污染对于眼表组织的损害和相应的潜在治疗靶点，指导临床上环境相关眼病的诊断与治疗。

More and more evidence indicate that air pollution can seriously damage human health and become a major cause of the global disease burden. The main component of air pollution, particulate matter, can penetrate the lungs and cardiovascular system, causing ischemic heart disease, pneumonia, chronic obstructive pulmonary disease, and even lung cancer, leading to an increase in the incidence and mortality rates related to air pollution. Urban particulate matter, as the main air pollution problem faced by urban residents, has been shown to be closely related to various inflammatory eye diseases, such as allergic conjunctivitis, keratitis, and dry eye. Our research further confirms that exposure to high concentration of urban particulate matter can also cause pathological structural changes and functional abnormalities in the meibomian gland, leading to inflammatory meibomian gland dysfunction. This review comprehensively summarizes the latest research on the eye surface diseases related to urban particulate matter and their pathogenic mechanisms, aims to elucidate the damage of air pollution to eye surface tissues, identify potential therapeutic targets, and guide the diagnosis and treatment of environmentally related eye diseases in clinical practice.

近年来，随着现代社会生活节奏的加快以及电子产品的普及，近视逐渐呈现低龄化、高发病率的趋势，成为不容忽视的公共卫生问题。动物和人类研究均发现，在近视的发展过程中，脉络膜表现出变薄的现象，并伴有血流量减少，这些变化与近视度数增加和眼轴增长呈正相关。研究表明，脉络膜厚度的变化不仅发生在近视初期，而是在近视进展阶段持续发生。此外，脉络膜血流量的调节也与近视的发生和发展密切相关，可能通过神经机制及生长因子的作用影响眼球的生长。光学相干断层扫描血管成像(optical coherence tomography angiography, OCTA)技术在探索近视进程中的脉络膜变化和血管功能方面展现了巨大的潜力。它能够提供无创性的脉络膜结构和血流信息，对于理解脉络膜在近视调控中的作用至关重要。未来的研究应当结合先进的OCTA技术，进一步探讨脉络膜在不同阶段近视中的具体变化及其背后的机制，特别是脉络膜血流调节与眼球生长之间的关系。深化对脉络膜在近视调控中作用的理解，将有助于开发有效的预防和控制措施，为近视防控策略提供理论依据。

In recent years, with the acceleration of the pace of life in modern society and the popularization of electronic products, myopia has gradually affected younger individuals and has a higher incidence rate, becoming a public health problem that cannot be ignored. Both animal and human studies have found that during the development of myopia, the choroid exhibits thinning and is accompanied by reduced blood perfusion. These changes are positively correlated with increased myopia and axial growth. Studies have shown that changes in choroidal thickness not only occur in the early stages of myopia, but also continue to occur in the progression stage of myopia. In addition, the regulation of choroidal blood flow is also closely related to the occurrence and development of myopia, which may affect the growth of the eyeball through the action of neural mechanisms and growth factors. Optical coherence tomography angiography (OCTA) technology has shown great potential in exploring choroidal changes and vascular function in the progression of myopia. It can provide non-invasive information on choroidal structure and blood flow, which is crucial for understanding the role of the choroid in the regulation of myopia. Future research should combine advanced OCTA technology to further explore the specific changes in the choroid in different stages of myopia and the underlying mechanisms, especially the relationship between choroidal blood flow regulation and eyeball growth. A better understanding of the role of choroid in myopia regulation will aid in developing effective prevention and control measures, providing a solid theoretical foundation for myopia prevention strategies.

目的：研究雌二醇(estradiol，E2)和丙酸睾酮(testosterone propionate，TP)对兔泪腺上皮细胞凋亡及对MMP-9蛋白表达的影响，探讨雌二醇及丙酸睾酮对干眼的作用机制。方法：体外培养兔泪腺上皮细胞，分别给予雌二醇及丙酸睾酮处理，双氧水(H₂O₂)诱导细胞凋亡，流式细胞仪检测细胞凋亡和免疫细胞化学法检测细胞MMP-9蛋白表达。实验分4组：凋亡对照组(AC组)、雌二醇组(E2组)、丙酸睾酮组(TP组)和空白对照组(BC组)。AC组只给予H₂O₂诱导凋亡，E2组给予1×10^-5mol/L雌二醇处理，TP组给予丙酸睾酮处理，BC组未加药物干预及未加H2O2诱导凋亡。结果：经H₂O₂诱导细胞凋亡后，泪腺上皮细胞早期凋亡率和MMP-9蛋白表达累积光密度值与BC组相比，AC组、E2组及TP组均显著增加；同比AC组，E2组及TP组细胞凋亡率和MMP-9蛋白表达量降低；E2组凋亡率及蛋白表达量比TP组明显降低；其差异均具有统计学意义(P<0.01)。结论：雌二醇和丙酸睾酮对H₂O₂诱导兔泪腺上皮细胞凋亡有一定的抑制作用，同时泪腺上皮细胞中MMP-9表达含量也降低，提示雌二醇和丙酸睾酮抑制兔泪腺上皮细胞凋亡的作用机制可能与MMP-9有关。

Objective: To investigate the effects of estradiol (E2) and testosterone propionate (TP) on apoptosis and matrix metalloproteinase-9 (MMP-9) expression in rabbit lacrimal gland epithelial cells. Methods: The rabbit lacrimal gland epithelial cells were cultured in vitro. H₂O₂ was used to induce apoptosis in cultured lacrimal gland epithelial cells and then treated with E2 and TP respectively. Cell apoptosis was detected by flow cytometer (FCM) and MMP-9 expression was evaluated by immunocytochemistry. There were four groups: apoptosis control group (AC), estradiol group (E2), testosterone propionate group (TP) and blank control group (BC) respectively. The cells of group AC were administrated with H₂O₂ only, group E2 and group TP with 1×10^_5 mol/L E2 and TP respectively and group BC in treated. Statistical analysis were performed with one-way analysis of variance (ANOVA test)using SPSS 16.0, P<0.05 was considered statistically significant. Results: Compared with group BC, the early cells apoptosis rate and integrated optical density of MMP-9 expression of lacrimal gland in group AC, E2 and TP increased significantly after the cells were induced by H₂O₂; Compared with group AC, group E2 and TP reduced; group E2 were significantly lower than group TP; the differences were all statistically significant (P<0.01). Conclusion: E2 and TP had a certain inhibitory effect on rabbit lacrimal gland epithelial cells apoptosis induced by H₂O₂. Meanwhile, MMP-9 expression of the lacrimal gland cells was decreased. These results indicated that E2 and TP on the apoptosis inhibitory mechanism of lacrimal gland cells may be related with MMP-9. 

青光眼是一组以视盘萎缩凹陷、视野缺损以及视力下降为共同特征的视神经退行性疾病，也是世界首位不可逆性致盲眼病，导致患者生活质量降低、引起极大卫生经济负担。但其发病机制尚不明确，促进房水排出从而降低眼内压力仍是目前减缓疾病进展的唯一治疗手段。房水排出的主要途径是经由小梁网进入Schlemm’ s管最后汇入巩膜外静脉，因此小梁网在调节房水排出以及平衡眼内压力方面发挥重要作用。近年以来体内以及体外房水排出测量技术和小梁网成像技术不断突破，众多研究表明小梁网存在压力依赖的节律性搏动，在房水的脉冲式排出中起到关键作用，但在青光眼中这种搏动随疾病的进展减弱甚至消失。文章将以小梁网的泵理论为核心，总结青光眼中房水排出的最新研究进展，并从恢复小梁网功能的角度出发探索可能有效的治疗策略，为青光眼的临床诊治提供新的思路。

青光眼是一组以视盘萎缩凹陷、视野缺损以及视力下降为共同特征的视神经退行性疾病，也是世界首位不可逆性致盲眼病，导致患者生活质量降低、引起极大卫生经济负担。但其发病机制尚不明确，促进房水排出从而降低眼内压力仍是目前减缓疾病进展的唯一治疗手段。房水排出的主要途径是经由小梁网进入Schlemm’ s管最后汇入巩膜外静脉，因此小梁网在调节房水排出以及平衡眼内压力方面发挥重要作用。近年以来体内以及体外房水排出测量技术和小梁网成像技术不断突破，众多研究表明小梁网存在压力依赖的节律性搏动，在房水的脉冲式排出中起到关键作用，但在青光眼中这种搏动随疾病的进展减弱甚至消失。文章将以小梁网的泵理论为核心，总结青光眼中房水排出的最新研究进展，并从恢复小梁网功能的角度出发探索可能有效的治疗策略，为青光眼的临床诊治提供新的思路。

       “锌”在青光眼研究舞台上正扮演着越来越重要的角色。糖皮质激素，作为人体内重要的激素之一，其对锌的调控已在诸多系统中被证实。研究发现，在糖皮质激素的影响下，小梁网中的锌离子转运受阻，导致细胞外基质降解失衡，从而干扰小梁网正常流出道功能，加重青光眼的病情。而视神经损伤后，锌离子在神经突触间的异常传递、不平衡分布与胞内异常累积影响视网膜神经节细胞存活和轴突的再生能力，进而损害视功能，可能成为青光眼视神经损伤发病及进展的关键因素。这些研究进展为视神经保护策略提供了新的视角，“锌”作为治疗靶点的潜力正在被逐步挖掘，通过调节锌水平来干预青光眼病理进程成为可能治疗手段。
       本期封面中将汉字“锌”设计为飞天舞者，其超越时空的永恒美感，呼应了“锌”在青光眼研究中突破传统、开辟新程的角色。轻盈与自由的飞天舞者，象征着“锌”在细胞内外穿梭，精妙调控生理功能，维系细胞的和谐与平衡，为青光眼患者带来新的治疗希望。

       “锌”在青光眼研究舞台上正扮演着越来越重要的角色。糖皮质激素，作为人体内重要的激素之一，其对锌的调控已在诸多系统中被证实。研究发现，在糖皮质激素的影响下，小梁网中的锌离子转运受阻，导致细胞外基质降解失衡，从而干扰小梁网正常流出道功能，加重青光眼的病情。而视神经损伤后，锌离子在神经突触间的异常传递、不平衡分布与胞内异常累积影响视网膜神经节细胞存活和轴突的再生能力，进而损害视功能，可能成为青光眼视神经损伤发病及进展的关键因素。这些研究进展为视神经保护策略提供了新的视角，“锌”作为治疗靶点的潜力正在被逐步挖掘，通过调节锌水平来干预青光眼病理进程成为可能治疗手段。

       本期封面中将汉字“锌”设计为飞天舞者，其超越时空的永恒美感，呼应了“锌”在青光眼研究中突破传统、开辟新程的角色。轻盈与自由的飞天舞者，象征着“锌”在细胞内外穿梭，精妙调控生理功能，维系细胞的和谐与平衡，为青光眼患者带来新的治疗希望。

青光眼是一种以视网膜神经节细胞(retinal ganglion cell, RGC)及其轴突的进行性变性和丢失为主要特征的眼病，是导致视力丧失的最常见原因。尽管其具体的发病机制尚未完全明确，但众所周知，眼内压升高是青光眼进展的主要危险因素。目前，通过药物和手术治疗降低眼内压是控制疾病进展的主要手段。他氟前列素因其能有效长期稳定地降低眼内压，且不良反应轻微、患者依从性高、无明显全身不良反应，已成为治疗原发性开角型青光眼及眼高压症的一线治疗药物。近年来的研究表明，他氟前列素除了具有降低眼内压的效果外，还可能具有神经保护作用。文章对他氟前列素的药理作用及其在神经保护方面的潜在效益进行综述，为开发更有效的治疗青光眼药物提供理论依据和科研基础。然而，目前缺乏充分的临床研究证据支持其神经保护效应，未来研究应进一步探索这一领域，以促进针对视神经保护的药物开发和基于视神经再生的视觉功能重建。

Glaucoma is characterized by the progressive degeneration and loss of retinal ganglion cells (RGC) and their axons,making it one of the most common causes of vision loss. Although the exact underlying mechanisms remain unclear, it is well known that elevated intraocular pressure (IOP) is a major risk factor for the progression of glaucoma. Currently, the primary means of controlling glaucoma involves reducing IOP through medication and surgery. Tafluprost, due to its effective and long-term ability to lower IOP, minimal side effects, high patient compliance, and absence of significant systemic side effects, has become the first-line treatment for primary open-angle glaucoma and ocular hypertension. Recent studies suggest that tafluprost may also have neuroprotective effects beyond its IOP-lowering effects. This article aims to review the pharmacological and potential neuroprotective effects of tafluprost, providing a theoretical basis and research foundation for developing more effective drugs for glaucoma treatment. However, there is still a lack of sufficient clinical evidence to support the neuroprotective effects of tafluprost, and further investigations are required to explore in this field to furnish critical theoretical backing for the development of drugs that target optic nerve protection and facilitate vision restoration through optic nerve regeneration.

糖皮质激素(glucocorticoid, GC)由于其抗炎特性被广泛用于治疗眼部炎症，而G C诱导性青光眼(glucocorticoid-induced glaucoma, GIG) 作为一种常见并发症，其发病机制长期受到关注。文章综述了锌在GIG中的关键作用及其调控机制，揭示了锌在青光眼发病机制中的重要角色。锌作为人体中含量第二丰富的过渡金属，对蛋白质结构、酶催化和细胞信号调节至关重要。GC对锌分布的调控作用在不同组织和细胞类型中表现出复杂性，影响锌的摄取和释放，进而参与青光眼的病理过程。锌通过影响小梁网细胞外基质(extracellular matrix, ECM)的降解和重塑，以及视网膜神经节细胞的存活和轴突再生，在GIG的发病机制中发挥着复杂的作用。文章同时介绍了体内锌调控的现有途径，包括补充锌和减少锌的策略，提供了潜在的治疗途径。未来的研究应深入探索锌在青光眼中的作用机制以及与GC的相互作用，评估锌补充或螯合在青光眼治疗中的安全性和有效性，以及开发新型锌递送和螯合系统，有助于全面揭示锌在青光眼中的作用及治疗潜力，以实现更加精准的防治方案，改善患者预后。

Glucocorticoid (GC) is widely used in the treatment of ocular inflammation for its anti-inflammatory propery. However, glucocorticoid-induced glaucoma (GIG) is a common complication, and its pathogenesis has been extensively studied. This review summarizes the crucial role of zinc in GIG and its regulatory mechanisms, highlighting zinc's significant involvement in the pathogenesis of glaucoma. Zinc, the second most abundant transition metal in the human body, is essential for protein structure, enzyme catalysis, and cell signaling regulation. The effects of GC on zinc distribution vary across different tissues and cell types, affecting zinc uptake and release, which may contribute to the pathological processes of glaucoma. Zinc influences the degradation and remodeling of the trabecular meshwork extracellular matrix and the survival and axonal regeneration of retinal ganglion cells, playing complex roles in the pathogenesis of GIG. We discuss available strategies for regulating zinc in vivo, including zinc supplementation and reduction strategies, providing potential therapeutic approaches. Future research should explore the mechanisms of zinc's role in glaucoma and its interaction with glucocorticoids, evaluate the safety and efficacy of zinc supplementation or chelation in glaucoma treatment, and develop novel zinc delivery and chelation systems. These efforts will help fully elucidate the role of zinc in glaucoma and its therapeutic potential, enabling more precise prevention and treatment strategies to improve patient outcomes.

原发性翼状胬肉是一种上皮下生长的非肿瘤性变性组织，其发病机制主要与紫外线照射有关，然而，原发性翼状胬肉的具体发病机制仍不明确。近年来，随着医学研究的不断深入，研究显示原发性翼状胬肉的发生发展与多种因素息息相关。病毒感染、氧化应激、炎症反应，抑癌基因失活、DNA 甲基化等因素已被证实与翼状胬肉发病机制有关。此外，凋亡和增殖蛋白的失衡、细胞外基质调节剂和上皮-间充质细胞转化等因素也都在原发性翼状胬肉的发病过程中扮演着重要的角色。这些均可能导致细胞生长和分裂的异常，进而诱发翼状胬肉的形成。然而，各个因素之间的相互作用以及它们在发病过程中的具体作用机制仍有待进一步研究。该文中笔者就当前原发性翼状胬肉的发病机制进行评述，深入探究原发性翼状胬肉的发病机制及不同相关因素在原发性翼状胬肉发病过程中的相互作用。了解不同因素在发病过程中的作用，可以为临床提供更加精准、有效的预防和治疗策略提供依据，为患者带来更好的治疗效果和更高生活质量。

Primary pterygium is a non-neoplastic degenerative tissue that grows subepithelially, and its pathogenesis is mainly related to ultraviolet exposure, however, the full mechanism of primary pterygium remains unclear. In recent years, with the development of medical research, it is found that the occurrence and development of primary pterygium are closely related to a variety of factors. Viral infection, oxidative stress, inflammatory response, inactivation of tumor suppressor genes, DNA methylation and other factors have been shown to be involved in the pathogenesis of pterygium. In addition, imbalances of apoptosis and proliferative proteins, extracellular matrix regulators, and epithelial-mesenchymal cell transformation also play important roles in the pathogenesis of primary pterygium. These can lead to abnormal cell growth and division, which in turn induces the formation of pterygium. However, the interaction between these factors and their specific mechanisms of action in the pathogenesis process still need to be further studied. In this article it reviews the current pathogenesis of primary pterygium, and deeply explores the pathogenesis of primary pterygium and the interaction of different related factors in the pathogenesis of primary pterygium. By understanding the role of different factors in the pathogenesis process, we can provide more precise and effective prevention and treatment strategies for clinical practice, and better treatment outcomes and quality of life for patients.