神经营养性角膜病变是一种与角膜神经退行性改变有关的疾病，角膜神经的知觉和营养功能受损，导致角膜上皮缺损、角膜溃疡甚至角膜穿孔。目前人工泪液、治疗性角膜绷带镜、泪点栓塞、羊膜移植，睑缘缝合等治疗措施仍是治疗神经营养性角膜病变的主要治疗方式，对于轻中度病变患者，具有较好的治疗效果，而对于重度病变患者，药物治疗及简单的手术干预治疗效果不佳，病情反复发作。由于重度神经营养性角膜病变患者的角膜神经完全消失，丧失角膜感觉，对未恢复角膜神经营养功能的角膜白斑或溃疡患者行角膜移植术，可能导致角膜移植术后上皮持续不愈合，因此恢复角膜神经营养功能是复明的重要保障手段。角膜神经移植术是重度神经营养性角膜病变患者恢复角膜神经营养功能，提高角膜知觉，改善角膜透明度的重要和有效的治疗方法。角膜神经移植术通过将具有正常功能的供体神经移植到麻痹眼角膜缘周围，使神经末梢重新长入角膜基质，恢复角膜知觉功能。随着角膜神经移植术的术式的不断改进，其良好的术后效果和优点已经渐渐突显。角膜神经移植术包括直接角膜神经移植和间接角膜神经移植，促使角膜神经重新生长，重建角膜神经的营养和知觉功能。角膜神经移植手术已有40年历史，1981年Samii等首次报告了角膜神经移植术，2009年Terzis等成功地实施了第1例直接角膜神经移植术，2014年Elbaz等进行了第1例以腓肠神经作为间置移植物的间接角膜神经移植。封面展示了神经营养性角膜病变患者未接受治疗前的和接受角膜神经移植术后的眼表角膜图像。由于角膜神经退行性改变，角膜失去神经支配，继而出现角膜上皮缺损，角膜缘新生血管形成，经角膜神经移植后，角膜上皮愈合，角膜透明度改善，同时角膜缘新生血管消退。

神经营养性角膜病变是一种与角膜神经退行性改变有关的疾病，角膜神经的知觉和营养功能受损，导致角膜上皮缺损、角膜溃疡甚至角膜穿孔。目前人工泪液、治疗性角膜绷带镜、泪点栓塞、羊膜移植，睑缘缝合等治疗措施仍是治疗神经营养性角膜病变的主要治疗方式，对于轻中度病变患者，具有较好的治疗效果，而对于重度病变患者，药物治疗及简单的手术干预治疗效果不佳，病情反复发作。由于重度神经营养性角膜病变患者的角膜神经完全消失，丧失角膜感觉，对未恢复角膜神经营养功能的角膜白斑或溃疡患者行角膜移植术，可能导致角膜移植术后上皮持续不愈合，因此恢复角膜神经营养功能是复明的重要保障手段。角膜神经移植术是重度神经营养性角膜病变患者恢复角膜神经营养功能，提高角膜知觉，改善角膜透明度的重要和有效的治疗方法。角膜神经移植术通过将具有正常功能的供体神经移植到麻痹眼角膜缘周围，使神经末梢重新长入角膜基质，恢复角膜知觉功能。随着角膜神经移植术的术式的不断改进，其良好的术后效果和优点已经渐渐突显。角膜神经移植术包括直接角膜神经移植和间接角膜神经移植，促使角膜神经重新生长，重建角膜神经的营养和知觉功能。角膜神经移植手术已有40年历史，1981年Samii等首次报告了角膜神经移植术，2009年Terzis等成功地实施了第1例直接角膜神经移植术，2014年Elbaz等进行了第1例以腓肠神经作为间置移植物的间接角膜神经移植。封面展示了神经营养性角膜病变患者未接受治疗前的和接受角膜神经移植术后的眼表角膜图像。由于角膜神经退行性改变，角膜失去神经支配，继而出现角膜上皮缺损，角膜缘新生血管形成，经角膜神经移植后，角膜上皮愈合，角膜透明度改善，同时角膜缘新生血管消退。

青光眼是一组以病理性眼压升高为主要危险因素的，以青光眼性神经萎缩和视野缺损为主要特征的全球首位不可逆性致盲眼病。超声睫状体成形术(UCP)是一种新型非侵入性青光眼治疗技术，其降眼压主要原理为利用高强度聚焦超声破坏睫状突上皮细胞以减少房水生成，并增加葡萄膜巩膜通道的房水流出。UCP适应证广泛，早期主要用于各类难治性青光眼患者，特别是晚期及绝对期患者，研究者发现其除降眼压外，还能够显著缓解该类患者的局部疼痛。近年来，UCP在未经手术治疗的青光眼患者和早、中期青光眼病例中，也表现出了良好的降眼压效果，同时显示出较少的并发症和较轻的术后反应，并可重复治疗。然而不同类型青光眼UCP疗效存在一定差异，且为达最佳治疗效果，其治疗需匹配恰当的探头型号以及适当的治疗扇区。现有较广泛应用于国外的基于眼轴和白到白参数的公式计算方法，测算精度并不适用于国人，然而精准度更高的模型法，其便捷性仍有待进一步提高。UCP虽可减少降眼压药物用量，但术后用药策略的调整仍可能导致眼压波动。综上，针对UCP手术的适应证选择、手术参数设计、疗效预判以及术后管理策略等，仍有待开展相关临床研究，以期为其临床应用提供更加可靠的依据。

青光眼是一组以病理性眼压升高为主要危险因素的，以青光眼性神经萎缩和视野缺损为主要特征的全球首位不可逆性致盲眼病。超声睫状体成形术(UCP)是一种新型非侵入性青光眼治疗技术，其降眼压主要原理为利用高强度聚焦超声破坏睫状突上皮细胞以减少房水生成，并增加葡萄膜巩膜通道的房水流出。UCP适应证广泛，早期主要用于各类难治性青光眼患者，特别是晚期及绝对期患者，研究者发现其除降眼压外，还能够显著缓解该类患者的局部疼痛。近年来，UCP在未经手术治疗的青光眼患者和早、中期青光眼病例中，也表现出了良好的降眼压效果，同时显示出较少的并发症和较轻的术后反应，并可重复治疗。然而不同类型青光眼UCP疗效存在一定差异，且为达最佳治疗效果，其治疗需匹配恰当的探头型号以及适当的治疗扇区。现有较广泛应用于国外的基于眼轴和白到白参数的公式计算方法，测算精度并不适用于国人，然而精准度更高的模型法，其便捷性仍有待进一步提高。UCP虽可减少降眼压药物用量，但术后用药策略的调整仍可能导致眼压波动。综上，针对UCP手术的适应证选择、手术参数设计、疗效预判以及术后管理策略等，仍有待开展相关临床研究，以期为其临床应用提供更加可靠的依据。

Ⅱ期人工晶状体(intraocular lens,IOL)植入常用于矫正先天性白内障摘除术后无晶状体眼状态。IOL屈光力计算是影响儿童Ⅱ期IOL植入术后视功能发育和改善的关键因素之一。现有IOL屈光力计算公式是基于成人有晶状体眼的数据研发，能准确预测成人眼IOL植入的屈光力，但是对儿童Ⅱ期IOL植入的屈光力预测准确性欠佳，主要原因包括：1)儿童II期植入术前为无晶状体眼，缺乏部分公式定义中的有晶状体眼的前房深度(是指从角膜前表面中央顶点到晶状体前表面的距离)和晶状体厚度。2)公式根据囊袋内植入IOL预测屈光力，但儿童Ⅱ期IOL睫状沟植入术在临床上应用更为广泛。当IOL植入睫状沟时有效晶状体位置发生前移，可能引起屈光预测误差。3)成人眼的发育已完成，目标屈光度多为正视或近视眼(-3.00 ~ +1.00 D)，但是儿童眼仍在发育，需针对其特性测算合适的远视目标屈光度(+0.50 ~ +12.00 D)以适应眼球发育引起的屈光变化。为使Ⅱ期IOL植入患儿达到术前预设的目标屈光度，对现有公式进行选择与优化至关重要。

Secondary intraocular lens (IOL) implantation is a common treatment for pediatric aphakia. The accurate prediction of IOL power calculation plays a pivotal role in the postoperative development and improvement of visual function for pediatric secondary IOL implantation. Current IOL power calculation formulas were developed based on data from adult phakic eyes and displayed good performance in adult population. However, the formulas showed poor performance in pediatric aphakic population due to the following reasons: 1) In these pediatric aphakic patients, the unavailability of phakic anterior chamber depth (the distance from corneal epithelium to the anterior surface of the lens) and lens thickness (LT) greatly limits the application of some IOL power calculation formulas. 2) IOL power calculation formulas predict the effective lens position on the basis of in-the-bag IOL implantation, whereas sulcus implantation is more widely used in pediatric secondary implantation. Effective lens position in capsular placement is more posterior to ciliary sulcus IOL placement. When applying the initial IOL power calculated for capsular implantation to sulcus implantation, it can lead to refractive errors. 3) Adult eyes have completed their development, with target refractions often being emmetropic or myopic (-3.00 ~ +1.00 D), while pediatric eyes are still developing, necessitating the calculation of an appropriate hyperopic (+0.50 ~ +12.00 D) target refraction to accommodate refractive changes due to ocular growth.To achieve the predetermined target refractive outcomes, the selection and optimization of IOL power calculation formulas is critically important for pediatric secondary IOL implantation.

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.