Cellular responses following retinal injuries and therapeutic approaches for neurodegenerative diseases

色素性视网膜炎 视网膜 视网膜变性 视网膜 神经科学 小胶质细胞 背景(考古学) 生物 黄斑变性 神经保护 医学 眼科 炎症 免疫学 古生物学
作者
Nicolás Cuenca,Laura Fernández‐Sánchez,Laura Campello,Victoria Maneu,Pedro de la Villa,Pedro Lax,Isabel Pinilla
出处
期刊:Progress in Retinal and Eye Research [Elsevier]
卷期号:43: 17-75 被引量:348
标识
DOI:10.1016/j.preteyeres.2014.07.001
摘要

Retinal neurodegenerative diseases like age-related macular degeneration, glaucoma, diabetic retinopathy and retinitis pigmentosa each have a different etiology and pathogenesis. However, at the cellular and molecular level, the response to retinal injury is similar in all of them, and results in morphological and functional impairment of retinal cells. This retinal degeneration may be triggered by gene defects, increased intraocular pressure, high levels of blood glucose, other types of stress or aging, but they all frequently induce a set of cell signals that lead to well-established and similar morphological and functional changes, including controlled cell death and retinal remodeling. Interestingly, an inflammatory response, oxidative stress and activation of apoptotic pathways are common features in all these diseases. Furthermore, it is important to note the relevant role of glial cells, including astrocytes, Müller cells and microglia, because their response to injury is decisive for maintaining the health of the retina or its degeneration. Several therapeutic approaches have been developed to preserve retinal function or restore eyesight in pathological conditions. In this context, neuroprotective compounds, gene therapy, cell transplantation or artificial devices should be applied at the appropriate stage of retinal degeneration to obtain successful results. This review provides an overview of the common and distinctive features of retinal neurodegenerative diseases, including the molecular, anatomical and functional changes caused by the cellular response to damage, in order to establish appropriate treatments for these pathologies.
最长约 10秒,即可获得该文献文件

科研通智能强力驱动
Strongly Powered by AbleSci AI
更新
大幅提高文件上传限制,最高150M (2024-4-1)

科研通是完全免费的文献互助平台,具备全网最快的应助速度,最高的求助完成率。 对每一个文献求助,科研通都将尽心尽力,给求助人一个满意的交代。
实时播报
玩家发布了新的文献求助10
1秒前
2秒前
笑南发布了新的文献求助10
3秒前
tess完成签到 ,获得积分10
3秒前
4秒前
5秒前
李健应助lqy555采纳,获得10
5秒前
今后应助飞奔的太阳采纳,获得10
6秒前
6秒前
hope完成签到,获得积分10
7秒前
7秒前
小团月完成签到 ,获得积分10
7秒前
8秒前
9209完成签到,获得积分10
8秒前
psh发布了新的文献求助10
9秒前
大模型应助陶醉琳采纳,获得10
9秒前
Viva应助gao456789采纳,获得30
9秒前
9秒前
欣慰水彤发布了新的文献求助10
10秒前
10秒前
11秒前
完美世界应助感动语蝶采纳,获得10
11秒前
大气依萱完成签到 ,获得积分10
11秒前
Sunnut完成签到,获得积分10
14秒前
上官若男应助陌君子筱采纳,获得10
14秒前
情怀应助笑南采纳,获得10
14秒前
欧阳宇完成签到,获得积分10
14秒前
15秒前
SciGPT应助想多睡会儿采纳,获得10
15秒前
jin驳回了ding应助
15秒前
amber发布了新的文献求助10
15秒前
乐观帅哥完成签到,获得积分10
17秒前
17秒前
谷雨完成签到,获得积分10
17秒前
Orange应助清爽灰狼采纳,获得10
18秒前
星辰大海应助小雄采纳,获得10
19秒前
修仙应助奥沙利楠采纳,获得10
19秒前
俊秀而完成签到,获得积分10
20秒前
奕奕发布了新的文献求助10
21秒前
tess发布了新的文献求助10
23秒前
高分求助中
Evolution 10000
Sustainability in Tides Chemistry 2800
юрские динозавры восточного забайкалья 800
Diagnostic immunohistochemistry : theranostic and genomic applications 6th Edition 500
Chen Hansheng: China’s Last Romantic Revolutionary 500
China's Relations With Japan 1945-83: The Role of Liao Chengzhi 400
Classics in Total Synthesis IV 400
热门求助领域 (近24小时)
化学 医学 生物 材料科学 工程类 有机化学 生物化学 物理 内科学 纳米技术 计算机科学 化学工程 复合材料 基因 遗传学 催化作用 物理化学 免疫学 量子力学 细胞生物学
热门帖子
关注 科研通微信公众号,转发送积分 3150106
求助须知:如何正确求助?哪些是违规求助? 2801196
关于积分的说明 7843534
捐赠科研通 2458660
什么是DOI,文献DOI怎么找? 1308585
科研通“疑难数据库(出版商)”最低求助积分说明 628556
版权声明 601721