Abstract：
Glaucoma, the leading cause of irreversible blindness worldwide, is a neurodegenerative disease characterized by chronic axonal damages and progressive loss of retinal ganglion cells, with increased intraocular pressure (IOP) as the primary risk factor. While current treatments focus solely on reducing IOP, understanding glaucoma through experimental models is essential for developing new therapeutic strategies and biomarkers for early diagnosis. Our research group developed an ocular hypertension rat model based on limbal plexus cautery, which provides significant glaucomatous neurodegeneration up to four weeks after injury. We evaluated long-term morphological, functional, and vascular alterations in this model. Our results showed that transient ocular hypertension, lasting approximately one week, can lead to progressive increase in optic nerve cupping and retinal ganglion cells loss. Remarkably, the pressure insult caused several vascular changes, such as arteriolar and venular thinning, and permanent choroidal vascular swelling. This study provides evidence of the longitudinal effects of a pressure insult on retinal structure and function using clinical modalities and techniques. The multifactorial changes reported in this model resemble the complex retinal ganglion cell degeneration found in glaucoma patients, and therefore may also provide a unique tool for the development of novel interventions to either halt or slow down disease progression.
摘要：
青光眼,全球不可逆失明的主要原因，是一种神经退行性疾病，其特征是慢性轴突损伤和视网膜神经节细胞的进行性丧失，以眼内压（IOP）升高为主要危险因素。虽然目前的治疗仅集中于降低IOP，通过实验模型了解青光眼对于开发新的治疗策略和早期诊断的生物标志物至关重要.我们的研究小组开发了一种基于角膜缘神经丛烧灼的高眼压大鼠模型，在损伤后4周内提供显著的青光眼性神经变性。我们评估了长期形态学，功能，和这个模型中的血管改变。我们的结果显示，短暂性高眼压，持续约一周,可导致视神经拔罐和视网膜神经节细胞的进行性增加。值得注意的是,压力损伤引起了一些血管变化，如小动脉和静脉变薄，和永久性脉络膜血管肿胀.这项研究使用临床方式和技术提供了压力损伤对视网膜结构和功能的纵向影响的证据。该模型中报道的多因素变化类似于青光眼患者中发现的复杂的视网膜神经节细胞变性，因此，也可能为开发新的干预措施以阻止或减缓疾病进展提供独特的工具。
