视网膜光损伤机制的研究进展  被引量:2

Research progress on the mechanism of retinal light injury

在线阅读下载全文

作  者:杨硕 王晨光[1] 齐首楠[1] Shuo Yang;Chen-Guang Wang;Shou-Nan Qi(Department of Ophthalmology,the Second Hospital of Jilin University,Changchun 130000,Jilin Province,China)

机构地区:[1]吉林大学第二医院眼科中心,吉林省长春市130000

出  处:《国际眼科杂志》2023年第6期938-942,共5页International Eye Science

基  金:吉林省科技发展计划项目(No.20210101297JC);吉林省教育厅项目(No.JJKH20180222KJ)。

摘  要:视网膜是一种高度专业化的组织,具有独特的结构及适应性,在所有不同类型的视网膜细胞中保持动态平衡对于维持视力至关重要。视网膜可能会暴露在各种环境损伤中,如光诱导的损伤,在进化过程中,视网膜细胞对各种损伤产生了适应性反应,这些反应共同恢复了细胞的动态平衡,并增加了组织对进一步损伤的抵抗力。然而过度光照则会导致视网膜组织内光感受器细胞、视网膜神经节细胞(RGC)、视网膜神经胶质细胞及视网膜色素上皮细胞(RPE)发生一系列病理改变,包括线粒体内活性氧(ROS)和Ca2+浓度增加、细胞凋亡、内质网应激、细胞自噬和炎症等,从而导致视网膜发生不可逆损伤。本文将对视网膜光损伤的发病机制和相关研究进展进行详细阐述,为未来防治视网膜光损伤提供研究方向。The retina is a highly specialized tissue with unique structure and adaptability.Maintaining dynamic balance in all different types of retinal cells is essential for maintaining vision.The retina may be exposed to a variety of environmental damage such as light-induced damage,and over the course of evolution,retinal cells have developed adaptive responses to various injuries that together restore dynamic cellular homeostasis and increase the resistance of the tissue to further damage.Howecer,excessive exposure to light can cause a series of pathological changes in photoreceptors,retinal ganglion cells(RGC),retinal glial cells and retinal pigment epithelium(RPE)cells,such as increased expression of reactive oxygen species(ROS)and Ca 2+in mitochondria,apoptosis,endoplasmic reticulum stress,autophagy and inflammation,etc.,leading to irreversible damage to the retina.In the present article,the possible pathogenesis and current related research progress of light-induced injury were reviewed,in order to provide research directions for the prevention and treatment of retinal light injury.

关 键 词:视网膜 光损伤 氧化应激 凋亡 炎症 

分 类 号:R774.1[医药卫生—眼科]

 

参考文献:

正在载入数据...

 

二级参考文献:

正在载入数据...

 

耦合文献:

正在载入数据...

 

引证文献:

正在载入数据...

 

二级引证文献:

正在载入数据...

 

同被引文献:

正在载入数据...

 

相关期刊文献:

正在载入数据...

相关的主题
相关的作者对象
相关的机构对象