小梁网
青光眼
神经保护
氧化应激
神经退行性变
视网膜神经节细胞
眼压
医学
神经科学
眼科
视网膜
疾病
生物
病理
内科学
作者
Sergio Claudio Saccà,Stefania Vernazza,Eugenio Luigi Iorio,Sara Tirendi,Anna Maria Bassi,Stefano Gandolfi,Alberto Izzotti
出处
期刊:Progress in Brain Research
日期:2020-01-01
卷期号:: 151-188
被引量:9
标识
DOI:10.1016/bs.pbr.2020.06.003
摘要
Glaucoma is a chronic neurodegenerative disease characterized by retinal ganglion cell loss. Although significant advances in ophthalmologic knowledge and practice have been made, some glaucoma mechanisms are not yet understood, therefore, up to now there is no effective treatment able to ensure healing. Indeed, either pharmacological or surgical approaches to this disease aim in lowering intraocular pressure, which is considered the only modifiable risk factor. However, it is well known that several factors and metabolites are equally (if not more) involved in glaucoma. Oxidative stress, for instance, plays a pivotal role in both glaucoma onset and progression because it is responsible for the trabecular meshwork cell damage and, consequently, for intraocular pressure increase as well as for glaucomatous damage cascade. This review at first shows accurately the molecular-derived dysfunctions in antioxidant system and in mitochondria homeostasis which due to both oxidative stress and aging, lead to a chronic inflammation state, the trabecular meshwork damage as well as the glaucoma neurodegeneration. Therefore, the main molecular events triggered by oxidative stress up to the proapoptotic signals that promote the ganglion cell death have been highlighted. The second part of this review, instead, describes some of neuroprotective agents such as polyphenols or polyunsaturated fatty acids as possible therapeutic source against the propagation of glaucomatous damage.
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