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.

干眼是以泪膜稳态丢失及伴随眼部不适症状为特征的最常见眼表疾病，泪膜不稳定、泪液高渗透性、眼表炎症及感觉神经异常为其主要病因。地夸磷索钠是一种P2Y2受体激动剂，能刺激黏蛋白及泪液分泌，其独特的作用机制为干眼的治疗开辟了新的方向，本文就地夸磷索钠近年的临床及基础研究进展作一综述。

Dry eye is one of the most common ocular surface diseases. It is characterized by a loss of homeostasis of the tear film, and accompanied by ocular symptoms, in which tear film instability and tear hyperosmolarity, ocular surface inflammation, and neurosensory abnormalities play major etiological roles. Diquafosol tetrasodium is a purinergic P2Y2 receptor agonist that promotes mucin and aqueous tear secretion. The unique pharmacological mechanism of diquafosol tetrasodium opens up a new direction for the medical therapies of dry eye. This article reviews the clinical therapeutic effect and research progress of diquafosol tetrasodium for the past few years.

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.

在晶状体纤维细胞分化的终末阶段，细胞核、线粒体、内质网及高尔基体等膜性细胞器会发生程序性的降解，这对晶状体透明性的维持至关重要。然而，晶状体细胞器降解过程的机制尚不明确。研究晶状体细胞器的降解过程可为阐明白内障的发病机制提供理论依据，也有望为晶状体再生提供新的干预靶点。本文就晶状体细胞器降解过程及其机制进行综述。

During terminal differentiation of lens fiber cells, nuclei and other organelles experience programmed elimination.This process is essential for the maintenance of lens transparency. However, the mechanisms underlying lens organelle degradation remain unclear. Identification of the mechanisms can provide a theoretical basis for elucidating the pathogenesis of cataract and is expected to reveal new intervention targets for lens regeneration. In this review, we discuss potential mechanisms and the process of lens organelle degradation.