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.
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。
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.
原发性获得性鼻泪管阻塞(primary acquired nasolacrimal duct obstruction，PANDO)是泪道阻塞性疾病中最常见的一类，好发于中老年女性，是眼科临床上的常见病、多发病，常继发急性或慢性泪囊炎的症状和体征，严重影响患者的日常工作和生活。本文对近年来PANDO可能的发病机制相关的研究进展、亟待解决的问题及未来研究的热点方向作一综述，旨在进一步加深对泪道阻塞性疾病发生发展的认识。
Primary acquired nasolacrimal duct obstruction (PANDO), which mainly occurs in the middle-aged and elderly women, is the most common type of obstructive diseases of the lacrimal duct, and it is also a common and frequently-occurring disease in ophthalmology. It constantly occurs secondary to various symptoms and signs of acute or chronic dacryocystitis, which seriously affects the daily work and life of patients. This article summarizes the research progress on the possible pathogenesis of PANDO in recent years, the urgent problems to be solvedand the hot research directions in the future, aiming to further deepen the understanding of the occurrence and development of lacrimal obstructive diseases.
眼睑皮脂腺癌是起源于眼睑部位皮脂腺体的恶性上皮性肿瘤，易复发、转移，主要治疗方式仍以手术切除为主，但患者整体预后并不理想，早期正确诊断和靶向治疗是改善患者预后和改进治疗的关键。眼睑皮脂腺癌临床表现复杂，早期容易误诊或漏诊进而延误治疗，病理检查是其诊断的金标准。此外，目前关于眼睑皮脂腺癌发病机制未完全阐明，癌发生发展的分子生物学过程尚未明确。因此，多方面了解眼睑皮脂腺癌发病机制为靶向治疗提供理论基础是十分必要的。本文主要从眼睑皮脂腺癌发病机制包括遗传因素、表观遗传、外源病毒感染、免疫逃逸、端粒酶学说等方面对眼睑皮脂腺癌作一综述。
Eyelid sebaceous gland carcinoma is a malignant epithelial tumor originating from eyelid sebaceous glands, which is prone to relapse and metastasis. The treatment mainly depends on surgical excision, but the overall prognosis of patients is not ideal. Early diagnosis and targeted therapy are the keys to improve the prognosis of patients.Due to its complex clinical manifestations, early misdiagnosis or missed diagnosis is easy to delay treatment, and pathological examination is still the gold standard for its diagnosis. In addition, the pathogenesis of eyelid sebaceous gland carcinoma is still unclear, and the molecular biological process of the occurrence and development is less understood. Therefore, it is very necessary to understand the pathogenesis of eyelid sebaceous gland carcinoma in various aspects to provide a theoretical basis for targeted therapy. In this paper, the pathogenesis of eyelid sebaceous gland carcinoma was reviewed from the aspects of gene , epigenetic, viral infection, immune escape, , telomerase theory and so on.
过敏性结膜炎经典的发病机制包括了IgE介导的I型超敏反应以及T淋巴细胞介导的IV型超敏反应，其中肥大细胞、肥大细胞脱颗粒释放的组胺、嗜酸性粒细胞等在过敏性结膜炎病理发展中发挥了重要作用。然而，临床发现针对上述机制的治疗药物临床疗效欠佳，有相当数量的过敏性结膜炎患者无法获得较好的生存质量，因此研究和阐明过敏性结膜炎的新机制，寻找新的治疗手段和药物靶点具有重要的临床意义。目前研究发现Th17细胞等多种炎性细胞和IL-17等细胞因子、过敏原介导神经调节机制、菌群失调机制、脂质介质作用方面可能与过敏性结膜炎发病相关，这对过敏性结膜炎新机制的研究有着重大的临床意义。本文将对过敏性结膜炎发病机制的新进展进行综述，以期为过敏性结膜炎的治疗提供新思路。
The classic pathogeneses of allergic conjunctivitis include type I hypersensitivity and type IV hypersensitivity, in which mast cells, eosinophils and some active substances such as histamine play important role. However, sincethe therapeutic drugs have not achieved satisfactory efficacy in clinical practices, a significant number of patients fail to achieve a good quality of life. The pathogenesis of allergic conjunctivitis remains to be further studied.Current studies have identified a variety of inflammatory cells such as Th17 cell and cytokines such as IL-17, the mechanisms of neuromodulation, flora dysregulation mechanisms, and lipid mediators that may be involved in the pathogenesis of allergic conjunctivitis, which has significant clinical implications for the study of mechanisms of allergic conjunctivitis. In this article, we will review the recent research progress of the pathogenesis of allergic conjunctivitis in order to provide new ideas for the treatment of allergic conjunctivitis.
睑板腺功能障碍(meibomian gland dysfunction，MGD)是一种慢性、弥漫性的睑板腺病变，通常以睑板腺终末导管的阻塞或分泌的睑脂数量或质量发生改变为特征，临床上可以引起泪膜异常、角膜上皮损害、眼部刺激等干眼表现。MGD病因复杂且受多种因素影响，因此MGD发病机制的研究对于指导临床工作至关重要。本文对研究MGD的动物模型进行了介绍，并根据一些基础研究对MGD相关的细胞及分子机制等方面进行综述。
Meibomian gland dysfunction (MGD) is a chronic and diffuse disease of the eyelid gland. It is usually characterized by obstruction of the terminal duct of the eyelid gland or changes in the quantity/quality of the eyelid fat secreted. It can clinically cause dry eye symptoms such as abnormal tear film, corneal epithelial damage and eye irritation. The etiology of MGD is complex and affected by a variety of factors. Therefore, the study on the pathogenesis of MGD is of great importance to guide clinical work. This article introduces the animal research model of MGD, and reviews the cellular and molecular mechanisms related to MGD based on some basic research.
