From DNA damage to functional changes of the trabecular meshwork in aging and glaucoma
详细信息 查看全文
- 作者：Sergio Claudio Saccà ; a ; sergio.sacca@hsanmartino.it" class="auth_mail" title="E-mail the corresponding author ; Stefano Gandolfib ; Alessandro Bagnisc ; Gianluca Mannid ; Gianluca Damontee ; Carlo Enrico Traversoc ; Alberto Izzottif
- 关键词：AC ; anterior chamber ; AH ; aqueous humor ; CLAN ; cross-linked actin network ; CM ; ciliary muscle ; CTM ; corneo-scleral trabecular meshwork ; ECM ; extracellular material/matrix ; EGL ; endothelial glycocalyx layer ; ET ; endothelin ; GSH ; glutathion ; HTG ; high-tension glaucoma ; IOP ; intraocular pressure ; JCT ; juxtacanalicular tissue ; LC ; lamina cribrosa ; LGN ; lateral geniculate nucleus ; LPA ; lysophosphatidic acid ; MGP ; inhibitor of calcification matrix Gla ; miRNAs ; microRNA ; NOS ; nitric oxide synthase ; NTG
- 刊名：Ageing Research Reviews
- 出版年：2016
- 出版时间：August 2016
- 年：2016
- 卷：29
- 期：Complete
- 页码：26-41
- 全文大小：3050 K
文摘
- •
Oxidative stress as pathogenetic mechanism for glaucoma is proposed.
- •
Trabecular meshwork impairment among senescence genetics and cellularity.
- •
The glaucomatous cascade include mitochondrial and endothelial dysfunction.
- •
Glaucomatous proteoma as biomarkers signals between anterior and posterior segment.