谷氨酸是哺乳动物中枢神经系统中的主要兴奋性神经递质，谷氨酸酶系统的持续激活会导致神经元的兴奋性毒性，进而引起神经元损伤和细胞死亡。兴奋性氨基酸转运体家族成员是一种多次跨膜蛋白，位于突触前膜、突触囊泡和神经胶质细胞膜上，也是一种高亲和力的钠钾依赖性载体，能够不断清除细胞外残留的谷氨酸，维持正常的突触内外谷氨酸水平和细胞内氧化还原稳态，对于保护细胞免受兴奋性毒性以及氧化应激损伤至关重要，兴奋性氨基酸转运体家族成员表水平达的失调与多种中枢神经系统疾病神经退行性变的发生和发展密切相关。在视网膜组织中，兴奋性氨基酸转运体家族成员广泛表达。目前大量研究表明，兴奋性氨基酸转运体家族成员广泛参与了青光眼、视网膜缺血再灌注损伤、年龄相关性黄斑变性等眼部疾病的发病，但具体机制有待进一步阐明。为此，文章综述了兴奋性氨基酸转运体家族成员的生理功能及其在相关眼科疾病发生和发展中作用的研究进展，为进一步阐明相关眼病发病的分子机制及新的防治靶点的发现提供新的视角。

SGlutamate is the primary excitatory neurotransmitter in the mammalian central nervous system. Persistent activation of the glutamatergic system can lead to excitotoxicity, resulting in neuronal damage and cell death. Members of the excitatory amino acid transporter (EAAT) family are multi-transmembrane proteins located on the presynaptic membrane, synaptic vesicles, and glial cell membranes. They function as high-affinity, sodium-potassium-dependent transporters, continuously clearing extracellular residual glutamate to maintain normal intra- and extracellular glutamate levels and intracellular redox homeostasis. This process is crucial for protecting cells from excitotoxicity and oxidative stress-induced damage. Dysregulation of EAATs is closely associated with the onset and progression of neurodegenerative diseases in the central nervous system. EAAT family members are widely expressed in retina. Numerous studies have demonstrated that these transporters are extensively involved in the pathogenesis of ocular diseases, including glaucoma, retinal ischemia-reperfusion injury, and age-related macular degeneration, although the specific mechanisms remain to be elucidated. Therefore, this article reviews the physiological functions of EAAT family members and their role in the development and progression of related ophthalmic diseases, providing new perspectives for further understanding the molecular mechanisms underlying these conditions and identifying novel therapeutic targets.

角膜屈光手术是目前屈光手术的主流术式，随着全飞秒、全激光手术方式的发展，手术变得更加安全精准，不仅角膜创伤小，术后恢复时间也进一步缩短。角膜具有屈光特性和典型的生物软组织力学特性，角膜力学特性不仅参与维持角膜形态，影响角膜手术尤其屈光手术的效果及预后，而且还与部分角膜疾病的发生和发展密切相关。近年来生物力学研究发展迅速，其在眼部疾病的诊疗中发挥着越来越重要的作用。角膜生物力学的变化与术前角膜的形态、不同手术方式的选择、术后角膜厚度的改变等多种因素相关，但手术导致的角膜自身形态改变是不可逆的，若术后角膜生物力学的变化较大，可能会引起医源性角膜扩张、继发性圆锥角膜等并发症的发生。为了规避术后角膜扩张风险和指导个性化的术式选择，了解角膜生物力学特性的影响至关重要。文章对角膜的基础结构、角膜生物力学特性、生物力学测量方法和不同术式及不同角膜瓣厚度术后生物力学变化的研究进展进行综述，为近视患者的个性化精准治疗提供理论指导。

Corneal refractive surgery is currently main stream of refractive surgery. With the development of femtosecond and laser surgery, the surgery has become safer and more accurate, resulting in less corneal trauma and a shorter postoperative recovery time. In recent years, biomechanics research has rapidly progressed, and its clinical application has gradually increased. The cornea not only possesses refractive properties but also exhibits typical biological soft tissue mechanical properties. Corneal mechanical properties not only play a role in maintaining corneal morphology but also influence the outcome and prognosis of corneal surgery, especially refractive surgery, and are closely related to the occurrence and development of some corneal diseases. Corneal refractive surgery involves cutting the cornea according to the patient's diopter, which disrupts the integrity of the cornea and inevitably affects its biomechanical stability. Changes in corneal biomechanics are associated with various factors, such as preoperative corneal morphology, the selection of different surgical methods, and postoperative changes in corneal thickness. However, the self-morphology changes caused by surgery are irreversible. If the postoperative changes in corneal biomechanics are significant, it may lead to complications such as postoperative corneal dilation and secondary keratoconus. To avoid postoperative iatrogenic corneal dilation and guide personalized surgical choice, it is crucial to understand the limits of influence of corneal biomechanical properties. This article reviews the research progress regarding corneal biomechanical properties and changes associated with corneal refractive surgery.

圆锥角膜（KC）是一种典型的扩张性眼病，以角膜扩张变薄并向前锥形突起为特征，严重时可致盲。KC三联征之一铁锈色Fleischer环，主要由上皮细胞基底膜周围的铁离子沉积组成。近年来，越来越多研究表明，铁稳态失衡可能与KC的发生和发展密切相关。KC患者泪液中铁相关蛋白的异常表达，提示铁稳态失衡可能是诱发KC的潜在致病机制。此外，角膜上皮细胞内铁稳态失衡导致细胞内铁离子异常积聚，进而引发活性氧和脂质过氧化物的大量生成，最终可能触发细胞铁死亡。从恢复铁稳态角度出发，螯合过量的铁离子和调控铁死亡过程关键靶点可能是未来KC潜在的治疗方法。目前关于铁稳态失衡导致KC发病的具体机制仍存在诸多谜团。随着相关研究的不断深入，有望通过改善角膜铁稳态失衡，为KC临床治疗带来新的思路和突破，也为KC患者提供更精准和个体化的治疗策略。

圆锥角膜（KC）是一种典型的扩张性眼病，以角膜扩张变薄并向前锥形突起为特征，严重时可致盲。KC三联征之一铁锈色Fleischer环，主要由上皮细胞基底膜周围的铁离子沉积组成。近年来，越来越多研究表明，铁稳态失衡可能与KC的发生和发展密切相关。KC患者泪液中铁相关蛋白的异常表达，提示铁稳态失衡可能是诱发KC的潜在致病机制。此外，角膜上皮细胞内铁稳态失衡导致细胞内铁离子异常积聚，进而引发活性氧和脂质过氧化物的大量生成，最终可能触发细胞铁死亡。从恢复铁稳态角度出发，螯合过量的铁离子和调控铁死亡过程关键靶点可能是未来KC潜在的治疗方法。目前关于铁稳态失衡导致KC发病的具体机制仍存在诸多谜团。随着相关研究的不断深入，有望通过改善角膜铁稳态失衡，为KC临床治疗带来新的思路和突破，也为KC患者提供更精准和个体化的治疗策略。

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.

剥脱综合征(exfoliation syndrome,XFS)以眼内异常纤维样物质沉积为特征，临床典型表现为裂隙灯下瞳孔缘和(或)晶状体前囊膜存在灰白色粉末状的剥脱物(exfoliation material,XFM)。XFM可阻塞小梁网引起剥脱性青光眼(exfoliaiton glaucoma,XFG)，并可通过房水循环进入血液，引起血管性损害。眼底病变视力损伤通常不可逆，XFM可进入眼底微血管及毛细血管，引起眼底结构和血管异常。基于光学相干断层成像技术的光学相干断层扫描(optical coherence tomography,OCT)及光学相干断层扫描血管成像(optical coherence tomography angiography,OCTA)以实时、非侵入性、高分辨率等优势，已广泛应用于眼底组织结构及血管病变检查。文章对XFS眼底病变在OCT和OCTA上的表现进行综述。

Exfoliation syndrome (XFS) was characterized by the abnormal deposition of the fber-like material intraocularly, and manifested as white or gray, powdery exfoliation material (XFM) on the pupillary border and (or) anterior lens capsule under slit lamp microscopy. XFM could obstruct the trabecular meshwork and cause exfoliation glaucoma (XFG). In addition, XFM that entered aqueous humor circulation could enter bloodstream and result in vascular damage. XFM could enter ocular fundus microvascular and capillary vessels, causing abnormalities of fundus structures and vessels. Optical coherence tomography (OCT) and optical coherence tomography angiography (OCTA), which were based on optical coherence tomography technology, had the advantages of real-time, non-intrusive and high resolution, et al. OCT and OCTA were widely used in detection of fundus structural and vascular abnormalities. Tis study was to review the fundus lesion of XFS on OCT and OCTA.

铁死亡是一种以铁沉积和脂质过氧化为主要特征的新型细胞死亡方式，目前在眼科方面的研究不断深入。视网膜因其本身功能和结构特点，易受到氧化应激的影响，而铁死亡已被证明在年龄相关性黄斑变性、青光眼、糖尿病性视网膜病变、视网膜色素变性等视网膜退行性疾病进程中发挥了重要作用。铁代谢途径作为铁死亡的主要调控方式之一，可通过调控细胞内铁稳态，介导芬顿反应形成脂质过氧化物，从而调控细胞铁死亡。转铁蛋白(transferrin,TF)、二价金属转运蛋白1(divalent metal transporter 1,DMT1)、铁蛋白(ferritin,FT)、铁转运蛋白1(ferroportin 1,FPN1)等铁代谢途径关键蛋白涉及细胞内铁离子的摄入、利用、储存、输出等多个方面，对细胞内铁稳态具有重要影响。通过调控铁代谢途径关键蛋白减少铁沉积而抑制铁死亡，可能成为延缓和治疗视网膜退行性疾病的新途径。文章对铁死亡概念、视网膜与铁死亡、铁死亡调控途径、铁代谢途径关键蛋白与视网膜退行性疾病的研究进展进行综述。

Ferroptosis, a novel form of cell death primarily characterized by iron deposition and lipid peroxidation, has been increasingly studied in the feld of ophthalmology. Te retina, due to its specifc functions and structure, is susceptible to oxidative stress. Ferroptosis has been proven to play a crucial role in the progression of retinal degenerative diseases such as age-related macular degeneration, glaucoma, diabetic retinopathy, and retinitis pigmentosa. Te iron metabolism pathway is one of the main regulatory mechanisms of ferroptosis, regulating intracellular iron homeostasis and mediating the formation of lipid peroxides through the Fenton reaction, thereby controlling cellular ferroptosis. Iron metabolism pathways, as one of the main regulatory mechanisms of ferroptosis, can regulate intracellular iron homeostasis and mediate the formation of lipid peroxides through the Fento reaction, thereby controlling cellur ferroptosis. Key proteins involved in iron metabolism pathways, including transferrin (TF), divalent metal transporter 1 (DMT1), ferritin (FT), and ferroportin 1 (FPN1), act as important roles in various aspects such as intracellular iron intake, utilization, storage, and export, exerting signifcant impacts on intracellular iron homeostasis. Regulating key proteins in iron metabolism pathways to reduce iron deposition and inhibiting ferroptosis may emerge aas a novel approach for delaying and treating retinal degenerative diseases. Tis article provides a comprehensive review of the concept of ferroptosis, the relationship between the retina and ferroptosis, the regulatory mechanisms of ferroptosis, and the research progress on key proteins in iron metabolism pathways and retinal degenerative diseases.

哺乳动物雷帕霉素靶蛋白(mammalian target of rapamycin,mTOR)是一种蛋白激酶，在体内主要参与营养水平、生长代谢的调节。mTOR是癌症、衰老和其他代谢相关病理性疾病的重要靶点，参与了增殖、转分化、自噬等多种生物学过程。眼被认为是具有免疫特权的区域，由于血管系统会影响视力，眼的血管系统位于中心光路以外。眼的许多区域都有将免疫细胞运输至发育不良、受损或衰老有关的病变部位的机制。尽管免疫应答主要是为了修复或保护自身，但是免疫细胞可能会分泌一些细胞因子，导致炎症或纤维化，进而损害视力。研究证实，mTOR与翼状胬肉、年龄相关性黄斑变性(age-related macular degeneration,AMD)、青光眼、白内障、糖尿病视网膜病变(diabetic retinopathy,DR)、眼部肿瘤等多种眼病密切相关。目前，mTOR抑制剂通常被用作免疫抑制剂，用于癌症的治疗，但mTOR抑制剂用于眼部疾病的报道尚少。因此，该文就mTOR信号通路在相关眼科疾病中的作用、调控机制、药物治疗等方面进行简要综述，为相关眼科疾病的病理机制与治疗提供思路，以便后续开展更深入的研究。

Mammalian target protein of rapamycin (mTOR) is a protein kinase that primarily involves in the regulation of nutrient levels andgrowth metabolism in vivo. mTOR serves as a crucial target for cancer, aging, and other metabolic related pathological diseases, participating in various biological processes such as proliferation, transdifferentiation, and autophagy. Te eye is considered an area with immune privilege, as the vascular system afects vision and is located outside the central light path. Many areas of the eye have mechanisms for transporting immune cells to the afected areas related to developmental, damaged, or aging. Although the immune response is primarily aimed at reparing or protecting itself, immune cells may secrete some cytokines, leading to infammation or fbrosis, which in turn can damage vision. Results from studies have confirmed that mTOR is closely related to pterygium, age-related macular degeneration (AMD), glaucoma, cataract, diabetic retinopathy (DR), eye tumors and other eye diseases. Currently, mTOR inhibitors are widely used as immunosuppressants and approved for cancer treatment; however, there are few reports on the use of mTOR inhibitors for eye diseases. Therefore, in the article it provides a brief overview of the role, regulatory mechanisms, and drug treatment of the mTOR signaling pathway in related ophthalmic diseases, providing ideas for the pathological mechanisms and treatment of related ophthalmic diseases, in order to carry out more in-depth research in the future.

年龄相关性黄斑变性(age-related macular degeneration,AMD)是一种发生在黄斑区的退行性变，其中湿性年龄相关性黄斑变性(wet age-related macular degeneration,wAMD)以黄斑区新生血管为主要病理特征，是导致老年人视力受损甚至失明的重要原因，视网膜下纤维化是wAMD最常见的自然后遗症，可导致光感受器、视网膜色素上皮(retinal pigment epithelial,RPE)和脉络膜毛细血管受损，导致不可逆转的中心视力丧失。多种基线特征被发现是视网膜下纤维化的危险因素，可用于预测早期视网膜下纤维化的发生。迄今为止，还没有有效的抗纤维化治疗方法，抗血管内皮生长因子(anti-vascular endothelia growth factor, anti-VEGF)治疗是wAMD的一线治疗方案，该治疗方法不能改善视网膜下纤维化，但及时启动治疗可能有助于预防或延缓纤维化的进展，目前多种靶向分子药物正被研发用于抗纤维化的治疗。该文综述了wAMD视网膜下纤维化的临床表现及意义、预测纤维化形成的基线特征、基本发病机制及潜在的抗纤维化治疗方法，旨在为临床诊治工作提供参考。

Age-related macular degeneration (AMD) is a degenerative disease of the macular, and wet age-related macular degeneration(wAMD) is mainly characterized by macular neovascularization, which is an important reason of visual impairment or even blindness in the elderly. Subretinal fibrosis is the most common natural sequelae of wAMD, which can lead to irreversible central vision loss by damaging photoreceptors, RPE, and choroidal capillaries. Multiple baseline features have been identified as the risk factors for subretinal fibrosis, which can be used to predict the early subretinal fibrosis. Heretofore, no anti fibrotic treatment method is effective. Anti vascular endothelial growth factor (anti VEGF) treatment is the first-line treatment for wAMD. This therapy cannot improve subretinal fibrosis, but timely initiation of treatment may help prevent or delay the progression of fibrosis. Currently, multiple targeted molecular drugs are being developed for anti fibrotic treatment. This article reviews the clinical manifestations and significance of subretinal fibrosis in wet age-related macular degeneration, baseline features for predicting the formation of fibrosis, basic pathogenesis, and potential anti-fibrosis treatment methods,aiming to provide reference for clinical diagnosis and treatment.

原发性干燥综合征(primary Sj?gren’s syndrome，SS)是一种主要累及外分泌腺体的自身免疫性疾病，患者通常因为严重的干眼症状首先就诊于眼科，大多数临床医师对原发性干燥综合征相关性干眼(Sj?gren’s syndrome dry eye disease，SS-DED)认识不足，可能导致漏诊和误诊。侵入性极小的客观检查及生物标志物的发展，将有助于发现SS-DED的真面目，并可能从新的角度阐释其发病机制，为其诊断、分类及治疗提供新的思路。SS-DED的治疗没有特效的药物，大多数患者需接受多种方法的治疗，以了解哪些方法最有效。

Primary Sj?gren’s syndrome is an autoimmune disease that mainly affects exocrine glands. Patients usually refer to ophthalmologists because of severe dry eye symptoms. Most clinicians have insufficient knowledge with dry eye disease associated with primary Sj?gren’s syndrome probably leading to misdiagnosis or missing the diagnosis.The diagnosis of Sj?gren’s syndrome dry eye disease (SS-DED) is difficult, but the extremely invasive objective examination and the development of biomarkers will help to understand this disease and explain its pathogenesis from a new perspective. There is no specific treatment for the SS-DED, and most patients should receive multiple treatments to select the optimal treatment.

微RNA-26b(microRNA-26b,miR-26b)是miR-26家族中的一员，作为基因表达调控因子，在细胞代谢、增殖、分化、凋亡、自噬、侵袭、转移等生物学过程中均发挥着重要的调控作用。近年来，随着对miR-26b研究的深入，研究者认识到miR-26b稳定存在于角膜、结膜上皮、晶状体、睫状体、小梁网、房水、玻璃体和视网膜等眼部组织中，且有越来越多的研究证实miR-26b在眼科疾病，例如翼状胬肉、白内障、增生性玻璃体视网膜病变、增生型糖尿病视网膜病变、年龄相关性黄斑变性等疾病的发生和发展中有着重要的调控作用。该文对近年miR-26b在眼科疾病方面的研究进行了综述，为探讨miR-26b在眼科疾病中发挥作用过程中的分子机制提供理论基础。

MicroRNA-26b (miR-26b) is a member of the miRNA-26 family. As a gene expression regulator, it plays an important regulatory role in biological processes such as cell metabolism, proliferation, differentiation, apoptosis, autophagy,invasion and metastasis. In recent years, with the in-depth study on miR-26b, researchers found that miR-26b stably exists in the cornea, conjunctival epithelium, lens, ciliary body, trabecular meshwork, aqueous humor, vitreous, retina and other ocular tissues. More study results confirmed that miR-26b acted on eye diseases, and played an important regulatory role in diseases occurrence and development, such as pterygium, cataract, proliferative vitreo retinopathy,proliferative diabetic retinopathy, age-related macular degeneration, etc. This article reviews the research progress of miR-26b in eye diseases recently, to provide a theoretical basis on molecular mechanisms involving in the role of miR-26b in eye diseases.