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.

年龄相关性黄斑变性(age-related macular degeneration, AMD)是导致老年人失明的主要原因之一，其特征为光感受器的死亡和视网膜色素上皮细胞的变性。该病的发病机制复杂，涉及遗传、环境和代谢等多种因素。细胞衰老是AMD的重要危险因素，表现为细胞在经历有限次数的分裂后进入永久性细胞周期停滞状态。随着年龄增长，衰老细胞的数量增加，并与多种年龄相关的慢性疾病密切相关。细胞衰老的潜在机制包括氧化应激、DNA损伤、线粒体功能障碍、自噬/线粒体自噬缺陷以及表观遗传改变等。在AMD中，色素上皮细胞、血管内皮细胞、Bruch膜、感光细胞和小胶质细胞等不同类型的细胞均表现出衰老及其相关变化。细胞衰老在AMD的发病机制中起着关键作用，涉及多种视网膜细胞类型和血管系统的退化。通过深入研究这些机制，期望能开发出更有效的治疗方法，以帮助患者恢复和保护视力。本文回顾了细胞衰老的生物学机制及其在AMD中的作用，深入探讨了不同细胞衰老引发AMD发病的具体机制，旨在为AMD的发病机制和治疗研究提供新思路。

Age-related macular degeneration (AMD) is a leading cause of blindness among the elderly, characterized by the degeneration of retinal pigment epithelial cells and the death of photoreceptors. The pathogenesis of AMD is complex, involving a multitude of factors, including genetic, environmental, and metabolic influences. Cellular senescence serves as a significant risk factor for AMD, where cells enter a permanent state of cell cycle arrest after a limited number of divisions. As age increases, the accumulation of senescent cells is closely associated with various age-related chronic diseases. Key mechanisms underlying cellular senescence include oxidative stress, DNA damage, mitochondrial dysfunction, defects in autophagy and mitophagy, and epigenetic alterations. In the context of AMD, various cell types-including pigment epithelial cells, vascular endothelial cells, cells of Bruch's membrane, photoreceptors, and microglia-exhibit signs of senescence and related changes. Cellular senescence plays a pivotal role in the pathogenesis of AMD, contributing to the degeneration of different retinal cell types and supporting vascular systems. By thoroughly investigating these mechanisms, there is hope for the development of more effective therapies aimed at restoring and protecting vision in affected patients. This article reviews the biological mechanisms of cellular senescence and its role in AMD, exploring how different cell types contribute to the disease's onset, with the goal of providing new insights into the pathogenesis and treatment of AMD.

Stargardt病(STGD1, OMIM#248200)是最常见的遗传性黄斑营养不良，是由ABCA4基因突变引起的常染色体隐性遗传病。该病通常在儿童晚期或成年早期发病，导致视力进行性、不可逆地损害。近年研究者在STGD1临床和分子特征以及潜在的病理生理学方面取得的重大进展，促成了许多已完成的、正在进行的和计划中的新疗法的人体临床试验。文章聚焦于STGD1的基因治疗研究进展。STGD1基因治疗的主要障碍是ABCA4基因序列过长以及ABCA4基因在光感受器细胞中的特异性转导效率不高。解决这一问题的关键是研究出具有大运载量和能高效将ABCA4基因转导进光感受器细胞的载体。目前STGD1的基因治疗策略主要包括腺相关病毒(adeno-associated viral, AAV)载体、慢病毒载体、纳米颗粒、光遗传学和反义寡核苷酸等。随着研究的深入，未来有望开发出针对STGD1的有效基因治疗方法，为患者带来新的治疗希望。该综述为临床应用和科学研究提供了宝贵的参考和思路。

Stargardt disease (STGD1, OMIM#248200) is the most common hereditary macular dystrophy, caused by mutations in the ABCA4 gene, and is an autosomal recessive inherited disorder. The disease typically manifests in late childhood or early adulthood, leading to progressive and irreversible visual impairment. Significant advances in understanding the clinical and molecular characteristics, as well as the underlying pathophysiology, have ultimately facilitated numerous human clinical trials of new therapies that have been completed, are ongoing, and are planned. This review focuses on the progress in gene therapy research for STGD1. The primary obstacle in STGD1 gene therapy is the lengthy sequence of the ABCA4 gene and the low efficiency of specific transduction of the ABCA4 gene into photoreceptor cells. The key to addressing this issue is to develop a vector with a large carrying capacity that can efficiently transduce the ABCA4 gene into photoreceptor cells. Current gene therapy strategies for STGD1 mainly include adeno-associated viral (AAV) vectors, lentiviral vectors, nanoparticles, optogenetics, and antisense oligonucleotides(AONs). With the deepening of research, it is hoped that effective gene therapy methods for STGD1 will be developed in the future, bringing new therapeutic hope to patients. This review provides valuable references and ideas for clinical applications and scientific research.

糖尿病性黄斑水肿(diabetic macular edema, DME)是糖尿病最常见和最严重的并发症之一，也是中青年劳动人群常见的致盲原因。DME病理生理机制复杂，是多种因素相互作用的结果，控制这些危险因素是降低发病率的关键。DME是全身病相关性眼病，其发生与发展受众多危险因素的影响，但此前文献对其总结不足，本文从全身因素及眼部因素两个方面就DME的危险因素进行综述。全身危险因素主要包括血糖控制欠佳、糖尿病病程长、高血压、血脂代谢紊乱、肥胖、肾功能异常、妊娠状态、降糖药物使用、贫血、阻塞性睡眠呼吸暂停低通气综合征、遗传因素、吸烟、饮酒、高血钙、低血镁等；而其眼部危险因素主要包括白内障、青光眼及玻璃体切割术、全视网膜激光光凝术、合并视网膜静脉阻塞和相关细胞因子等。深入认识和理解这些危险因素，有助于更好地预防和早期治疗DME，同时为治疗糖尿病视网膜病变过程中控制DME进展提供指引和参考。但是，其中一部分因素还存在一定争议，更多的DME危险因素仍有待进一步探索，期望在不久的将来，更多基础和前瞻性临床研究为DME危险因素及治疗提供高质量的证据。

Diabetic macular edema (DME) is one of the most common and severe complications of diabetes, and it is a leading cause of blindness in the working-age population. The pathophysiology of DME is complex, resulting from the interplay of various factors. Controlling these risk factors is crucial in reducing the incidence of DME. As a systemic diseaserelated ocular condition, the onset and progression of DME are influenced by numerous risk factors. However, previous literature has provided insufficient summaries of these factors. This review aims to summarize the risk factors for DME from both systemic and ocular perspectives. The systemic risk factors primarily include poor glycemic control, prolonged duration of diabetes, hypertension, dyslipidemia, obesity, renal dysfunction, pregnancy, the use of hypoglycemic medications, anemia, obstructive sleep apnea-hypopnea syndrome, genetic factors, smoking, alcohol consumption, hypercalcemia, and hypomagnesemia. On the other hand, ocular risk factors include cataracts, glaucoma and vitrectomy, panretinal photocoagulation, coexisting retinal vein occlusion, and related cytokines. A deeper understanding of these risk factors will aid in the better prevention and early treatment of DME, while also providing guidance and reference for controlling the progression of DME during the treatment of diabetic retinopathy. However, some of these factors remain controversial, and additional DME risk factors still need to be explored. It is hoped that, in the near future, more 

foundational and prospective clinical studies will provide high-quality evidence on DME risk factors and treatments.

脉络膜是视网膜的主要血供来源，脉络膜血管系统为眼内最大、最重要的血管系统，在给外层视网膜供血方面起着至关重要的作用。脉络膜是一个动态、多功能性结构，其生理性特性受多种因素影响。这些因素包括年龄、性别、解剖位置、眼轴长度、昼夜节律与饮酒等。脉络膜涡静脉根据解剖学位置可分为眼内、巩膜内和眼外三大部分，又进一步分为脉络膜静脉、壶腹前部、壶腹、壶腹后部、巩膜入口、巩膜内通道、巩膜出口和巩膜外涡静脉八个区域。在正常眼中，涡静脉的类型不仅限于传统认知中出口位于赤道部近睫状体平坦部的涡静脉，研究发现还存在出口位于后极部的后极部涡静脉。根据涡静脉的形态及解剖特点，涡静脉又分为四类：缺失型涡静脉、不完整型涡静脉、完整型涡静脉、完整型涡静脉伴壶腹。文章旨在阐述正常人眼的脉络膜血流及涡静脉解剖基础，以深入了解正常状态下的脉络膜特征，这不仅有助于辨别脉络膜的病理性变化，且对脉络膜相关眼部疾病的诊断与鉴别诊断有重要价值。

The choroid is the primary source of blood supply for the retina. As the largest and most important vascular system within the eye, the choroidal vasculature plays a crucial role in providing blood to the outer retina. The choroid is a dynamic, multifunctional structure whose physiological characteristics are influenced by a variety of factors. These factors include age, gender, anatomical location, axial length of the eye, circadian rhythm, and alcohol consumption, among others. Choroidal vortex veins can be anatomically divided into three main parts: intraocular, scleral, and extraocular. Furthermore, they can be subdivided into eight distinct regions: choroidal veins, pre-ampulla, ampulla, post-ampulla, scleral entrance, intrascleral canal, scleral exit, and extrascleral vortex vein. In the healthy eye, the types of vortex veins are not limited to the traditionally recognized veins with exits near the ciliary body pars plana in the equatorial region. Recent research has revealed the existence of posterior vortex veins with exits in the posterior pole of the eye. Based on the morphology and anatomical characteristics of vortex veins, they can be further classified into four types:absent vortex veins, incomplete vortex veins, complete vortex veins, complete vortex veins with ampulla. This paper aims to elucidate the blood flow and vortex veins anatomical foundation of the choroid in normal human eyes. Understanding these characteristics in a healthy state will aid in identifying pathological changes in the choroid, which is of significant value for the diagnosis and differential diagnosis of ocular diseases.

马方综合征 (Marfan syndrome, MFS) 是一种由原纤维蛋白-1(fibrillin-1,FBN-1)突变引起的全身性遗传性疾病，FBN-1基因突变与MFS相关表型的联系相关，目前已报道的MFS常见的眼部表现包括角膜扁平、长眼轴、晶状体异位以及视网膜病变等异常，这些眼部异常将对MFS患者的视力产生影响，如角膜异常可影响角膜高阶像差的异常，可能导致近视或散光等屈光状态异常，从而影响视觉质量，损害视力清晰度。此外，MFS的眼底血管病变，也可能导致MFS患者的视力丧失，研究发现，MFS视网膜血管及脉络膜血管的密度较正常人减少，并与最佳矫正视力相关，由于光感受器的代谢与营养供应与视网膜及脉络膜血管息息相关，血管异常可能与视力损失相关。由于MFS患者存在视力损害的风险，其早期诊断和治疗尤为重要，因此，了解MFS眼部病变的特点及其对视力的影响，对制定针对MFS眼病的治疗方案具有重要的意义。另外，由于MFS眼部异常与FBN1基因突变相关，其基因突变类型多样，致病机制复杂，总结MFS眼部特点对其发病机制的继续探索有一定的指导作用，因此，文章拟就MFS患者眼部生物学参数特点及其对视力的影响这一领域国内外的相关研究进展进行综述。

Marfan syndrome (MFS) is a systemic hereditary disease caused by fibrillin-1 (FBN-1) mutations. FBN-1 gene mutations are associated with MFS-related phenotypes. Common ocular manifestations of MFS reported so far include corneal flattening, long axial length, ectopia lentis, and retinal abnormalities. These ocular abnormalities will affect the vision of MFS patients. For example, corneal abnormalities can affect abnormalities in corneal higher-order aberrations, which may lead to abnormal refractive states such as myopia or astigmatism, thereby affecting visual quality and compromising visual acuity. In addition, retinal vascular abnormalities may also lead to vision loss in MFS patients. Studies have found that the density of retinal and choroidal blood vessels in MFS patients is lower than that in normal individuals and is associated with best corrected visual acuity. Given the close relationship between the metabolism and nutrient supply of photoreceptors and retinal and choroidal vasculature, vascular abnormalities may be linked to visual impairment. Since MFS patients are at risk of visual impairment, early diagnosis and treatment are particularly important. Therefore, understanding the characteristics of ocular manifestations in MFS and their impact on vision is crucial for devising effective treatment strategies for MFS-related ocular conditions. Additionally, as ocular abnormalities in MFS are linked to mutations in the FBN1 gene, which exhibit diverse mutation types and complex pathogenic mechanisms, summarizing the ocular features of MFS can provide valuable insights for further exploration into its pathogenesis. Therefore, this article aims to review the progress of domestic and international research on the ocular biological parameters of MFS patients and their impact on vision.

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。