State Key Laboratory of Ophthalmology, Zhongshan Ophthalmic Center, Sun Yat-Sen University, Guangzhou, Guangdong 510060, China.
Chin Med J (Engl). 2013 Nov;126(22):4358-65.
To gain insight into the potential mechanism of mitochondria dysfunction in pathogenesis, progression and therapeutic management of glaucoma.
The data used in this review were mainly published in English from 2000 to present obtained from PubMed. The search terms were "mitochondria", "glaucoma" and "trabecular meshwork" or "retinal ganglion cells".
Articles studying the mitochondria-related pathologic mechanism and treatment of glaucoma were selected and reviewed.
Mitochondrial dysfunction or injury was demonstrated in different eye tissue of glaucoma. A variety of potential injuries (light, toxic materials, oxidative injury, mechanical stress, aging, etc.) and the inherent DNA defects are deemed to cause mitochondrial structural and functional destruction in trabecular meshwork cells, retinal ganglion cells, etc. of glaucoma. In addition, various new experimental and therapeutic interventions were used to preserve mitochondrial function, which may be useful for protecting against optic nerve degeneration or reducing the death of retinal ganglion cells in glaucoma.
Mitochondria play an important role in the pathogenesis of glaucoma, various strategies targeting mitochondrial protection might provide a promising way to delay the onset of glaucoma or protect RGCs against glaucomatous damage.
深入了解线粒体功能障碍在青光眼发病机制、进展和治疗管理中的潜在机制。
本综述中使用的数据主要来源于 2000 年至今发表的英文文献，来自 PubMed。检索词为“线粒体”“青光眼”和“小梁网”或“视网膜神经节细胞”。
选择并回顾了研究青光眼与线粒体相关病理机制和治疗的文章。
在不同的青光眼眼组织中都证明了线粒体功能障碍或损伤。各种潜在的损伤（光、有毒物质、氧化损伤、机械应激、衰老等）和内在的 DNA 缺陷被认为会导致小梁网细胞、视网膜神经节细胞等的线粒体结构和功能破坏。此外，还使用了各种新的实验和治疗干预措施来维持线粒体功能，这可能有助于防止视神经变性或减少青光眼患者视网膜神经节细胞的死亡。
线粒体在青光眼的发病机制中起重要作用，针对线粒体保护的各种策略可能为延缓青光眼的发生或保护 RGC 免受青光眼损伤提供有前景的方法。
