摘要
缺血性视网膜病变会导致微血管损伤、炎症进展和新生血管出现,是造成视力损伤的重要原因。在这些病理过程中,视网膜胶质细胞的作用不容忽视,它们用途广泛,与各类细胞相互作用,共同维持视网膜内环境稳定并限制疾病进展。因此,胶质细胞的活化和增生几乎是所有视网膜疾病中普遍存在的反应。其中,小胶质细胞和Müller细胞作为两种主要的内源性视网膜胶质细胞,彼此影响、共同作用甚至相互依存,能够通过不同反应发生形态及功能转换,决定视网膜的损伤程度。这些反应不仅关乎疾病进展程度,也对维持神经元及光感受器存活至关重要。了解缺血性视网膜病变中小胶质细胞与Müller细胞间可能存在的交互作用,有望为寻找更具有针对性的早期治疗靶点提供思路。
Ischemic retinopathy,resulting in multiple lesions like microvasculature damage,inflammation and neovascularization,is a major contributor of vision damage.In these pathological changes,retinal glia cannot be ignored in the development of retinopathy.They constitute a highly versatile population that interacts with various cells to maintain homeostasis and limit disease.Therefore,glial activation and gliosis are strikingly ubiquitous responses to almost every form of retinal disease.Both of microglial cells and Müller cells are major intrinsic retinal glial cells and they are in close relationship,which means they can influence each other,make joint action or even become interdependent.They exhibit morphological and functional changes to have an impact on degree of retinal injury through different responses,which mediated by glial cells are important not only for course of disease progression,but also for the maintenance of neuronal and photoreceptor survival.Thus,defining the mechanisms that underlie communications between microglial cells and Müller cells could enable the development of more selective therapeutic targets,with great potential clinical applications.
作者
高爽
沈玺
Gao Shuang;Shen Xi(Department of Ophthalmology,Ruijin Hospital,Shanghai Jiao Tong University School of Medicine,Shanghai 200025,China)
出处
《中华眼底病杂志》
CAS
CSCD
北大核心
2020年第1期74-78,共5页
Chinese Journal of Ocular Fundus Diseases