Shinozaki Youichi, Koizumi Schuichi
Department of Neuropharmacology, Interdisciplinary Graduate School of Medicine, University of Yamanashi.
Nihon Yakurigaku Zasshi. 2020;155(2):87-92. doi: 10.1254/fpj.19120.
Glaucoma, progressive optic neuropathy, is the first cause of blindness in Japan. Blindness in this disease is induced by damages or degeneration of retinal ganglion cells (RGCs), retinal neurons transmit visual information to brain. An elevated intraocular pressure (IOP) is widely recognized as one of the most important risk factors and that IOP directly damages RGCs by mechanical stress, however, accumulating evidences have shown that a majority of Japanese patients for primary open angle glaucoma shows normal level of IOP. Thus, new target for glaucoma pathology is emerged. In this issue, we introduce potential roles of glial cells for pathogenesis of glaucoma. In the CNS, reactive gliosis has been recognized in a variety of neurodegenerative diseases. Such glial activation is also found in retinae of human glaucoma patients and animal models. Importantly, glial activation precedes RGS degeneration, indicating the possibility that reactive glial cells actively contribute to pathogenesis of glaucoma. In this issue, we will focus on macroglial cells such as Muller cells and astrocytes, and discuss their roles in glaucoma.
青光眼,一种进行性视神经病变,是日本失明的首要原因。该疾病导致的失明是由视网膜神经节细胞(RGCs)的损伤或退化引起的,视网膜神经节细胞是将视觉信息传递到大脑的视网膜神经元。眼内压(IOP)升高被广泛认为是最重要的危险因素之一,并且眼内压通过机械应力直接损害视网膜神经节细胞,然而,越来越多的证据表明,大多数日本原发性开角型青光眼患者的眼内压水平正常。因此,出现了青光眼病理的新靶点。在本期中,我们介绍了神经胶质细胞在青光眼发病机制中的潜在作用。在中枢神经系统中,在多种神经退行性疾病中都发现了反应性胶质增生。在人类青光眼患者和动物模型的视网膜中也发现了这种神经胶质细胞激活。重要的是,神经胶质细胞激活先于视网膜神经节细胞退化,这表明反应性神经胶质细胞可能积极参与青光眼的发病机制。在本期中,我们将聚焦于如穆勒细胞和星形胶质细胞等大神经胶质细胞,并讨论它们在青光眼中的作用。