内质网（ER）作为蛋白质内稳态的质量控制细胞噬，称为“蛋白质稳态”。蛋白质质量控制系统包括ER相关的降解、蛋白质伴侣和自噬。当ER中积累了错误折叠和未折叠的蛋白质，破坏了蛋白质稳态时，ER应激将被激活。ER应激通过启动蛋白激酶R样ER激酶、活化转录因子6和肌醇需求酶1来激活适应性未折叠蛋白质应答，以恢复蛋白质稳态。ER应激是多方面的，并作用于表观遗传水平的各个方面，包括转录和蛋白质加工。积累的数据表明，ER应激在蛋白质稳态和涉及眼部疾病的其他多样功能中发挥着关键作用，如青光眼、糖尿病视网膜病变、老年性黄斑变性、色素性视网膜炎、无色觉症、白内障、眼部肿瘤、眼表疾病和近视。本综述从ER应激的角度总结了上述眼部疾病的分子机制。药物（化学药物、神经营养因子和纳米颗粒）、基因治疗和干细胞治疗通过缓解ER应激来治疗眼部疾病。我们阐述了针对ER应激的疗法的进展，为眼部疾病提供了新的治疗策略。© 2023. 四川大学华西医院。

The endoplasmic reticulum (ER) functions as a quality-control organelle for protein homeostasis, or "proteostasis". The protein quality control systems involve ER-associated degradation, protein chaperons, and autophagy. ER stress is activated when proteostasis is broken with an accumulation of misfolded and unfolded proteins in the ER. ER stress activates an adaptive unfolded protein response to restore proteostasis by initiating protein kinase R-like ER kinase, activating transcription factor 6, and inositol requiring enzyme 1. ER stress is multifaceted, and acts on aspects at the epigenetic level, including transcription and protein processing. Accumulated data indicates its key role in protein homeostasis and other diverse functions involved in various ocular diseases, such as glaucoma, diabetic retinopathy, age-related macular degeneration, retinitis pigmentosa, achromatopsia, cataracts, ocular tumors, ocular surface diseases, and myopia. This review summarizes the molecular mechanisms underlying the aforementioned ocular diseases from an ER stress perspective. Drugs (chemicals, neurotrophic factors, and nanoparticles), gene therapy, and stem cell therapy are used to treat ocular diseases by alleviating ER stress. We delineate the advancement of therapy targeting ER stress to provide new treatment strategies for ocular diseases.© 2023. West China Hospital, Sichuan University.