Department of Medicine Endocrinology, University of Oklahoma Health Sciences Center, Oklahoma City, OK, USA.
Department of Ophthalmology, Xiangya Hospital, Central South University, Changsha, China.
Adv Exp Med Biol. 2019;1185:469-473. doi: 10.1007/978-3-030-27378-1_77.
The concept that Müller glia (MG) are major retinal supporting cells for neuroprotection under various stresses is well established. However, the detailed molecular and cellular mechanisms of MG-mediated neuroprotection remain elusive. Particularly, the role and mechanism of MG in neuroprotection under diabetic and hypoxic stresses are largely unknown. In this article, we will discuss the role and mechanisms of a major growth factor, vascular endothelial growth factor (VEGF), in mediating MG viability and its potential impact on neuronal integrity in diabetes and hypoxia, demonstrate results on alternative mechanisms to VEGF signaling for MG and neural protection, and highlight the relevance of our work to the treatment of neovascular age-related macular degeneration, diabetic retinopathy, wet age-related macular degeneration, and other hypoxic retinal vascular diseases.
Müller 胶质细胞（MG）是多种应激下视网膜主要的神经保护支持细胞，这一概念已得到广泛认可。然而，MG 介导的神经保护的详细分子和细胞机制仍不清楚。特别是 MG 在糖尿病和缺氧应激下的神经保护作用及其机制在很大程度上仍是未知的。在本文中，我们将讨论一种主要生长因子血管内皮生长因子（VEGF）在调节 MG 活力及其对糖尿病和缺氧状态下神经元完整性的潜在影响中的作用和机制，展示替代 VEGF 信号通路的 MG 和神经保护的机制，并强调我们的工作与治疗新生血管性年龄相关性黄斑变性、糖尿病性视网膜病变、湿性年龄相关性黄斑变性和其他缺氧性视网膜血管疾病的相关性。
