de Hoz Rosa, Rojas Blanca, Ramírez Ana I, Salazar Juan J, Gallego Beatriz I, Triviño Alberto, Ramírez José M
Instituto de Investigaciones Oftalmológicas Ramón Castroviejo, Universidad Complutense de Madrid, 28040 Madrid, Spain; Departamento de Oftalmología y ORL, Facultad de Óptica y Optometría, Universidad Complutense de Madrid, 28037 Madrid, Spain.
Instituto de Investigaciones Oftalmológicas Ramón Castroviejo, Universidad Complutense de Madrid, 28040 Madrid, Spain; Departamento de Oftalmología y ORL, Facultad de Medicina, Universidad Complutense de Madrid, 28040 Madrid, Spain.
Biomed Res Int. 2016;2016:2954721. doi: 10.1155/2016/2954721. Epub 2016 May 18.
Due to their permanent and close proximity to neurons, glial cells perform essential tasks for the normal physiology of the retina. Astrocytes and Müller cells (retinal macroglia) provide physical support to neurons and supplement them with several metabolites and growth factors. Macroglia are involved in maintaining the homeostasis of extracellular ions and neurotransmitters, are essential for information processing in neural circuits, participate in retinal glucose metabolism and in removing metabolic waste products, regulate local blood flow, induce the blood-retinal barrier (BRB), play fundamental roles in local immune response, and protect neurons from oxidative damage. In response to polyetiological insults, glia cells react with a process called reactive gliosis, seeking to maintain retinal homeostasis. When malfunctioning, macroglial cells can become primary pathogenic elements. A reactive gliosis has been described in different retinal pathologies, including age-related macular degeneration (AMD), diabetes, glaucoma, retinal detachment, or retinitis pigmentosa. A better understanding of the dual, neuroprotective, or cytotoxic effect of macroglial involvement in retinal pathologies would help in treating the physiopathology of these diseases. The extensive participation of the macroglia in retinal diseases points to these cells as innovative targets for new drug therapies.
由于神经胶质细胞与神经元永久且紧密相邻,它们对视网膜的正常生理功能执行着至关重要的任务。星形胶质细胞和米勒细胞(视网膜大胶质细胞)为神经元提供物理支持,并为其补充多种代谢物和生长因子。大胶质细胞参与维持细胞外离子和神经递质的稳态,对神经回路中的信息处理至关重要,参与视网膜葡萄糖代谢并清除代谢废物,调节局部血流,诱导血视网膜屏障(BRB)形成,在局部免疫反应中发挥重要作用,并保护神经元免受氧化损伤。针对多种病因的损伤,神经胶质细胞会通过一种称为反应性胶质增生的过程做出反应,试图维持视网膜的稳态。当功能失调时,大胶质细胞可成为主要的致病因素。在包括年龄相关性黄斑变性(AMD)、糖尿病、青光眼、视网膜脱离或色素性视网膜炎等不同的视网膜病变中都已描述了反应性胶质增生。更好地理解大胶质细胞参与视网膜病变的双重、神经保护或细胞毒性作用将有助于治疗这些疾病的病理生理学。大胶质细胞在视网膜疾病中的广泛参与表明这些细胞是新药治疗的创新靶点。