Targeting mitochondrial function to protect against vision loss

被引:9
作者
Chhetri, Jamuna [1 ]
Gueven, Nuri [1 ]
机构
[1] Univ Tasmania, Div Pharm, Sch Med, Fac Hlth, Hobart, Tas 7001, Australia
关键词
Drugs; eyes; inherited mitochondrial disease; mitochondria; neurodegenerative disease; ocular disease; short-chain quinones; vision; HEREDITARY OPTIC NEUROPATHY; GANGLION-CELL DEATH; NONSTEROIDAL ANTIINFLAMMATORY DRUGS; RETINAL-PIGMENT EPITHELIUM; OPEN-ANGLE GLAUCOMA; COMPLEX-I; OXIDATIVE STRESS; WOLFRAM-SYNDROME; COHERENCE TOMOGRAPHY; DIABETIC-RETINOPATHY;
D O I
10.1517/14728222.2015.1134489
中图分类号
R9 [药学];
学科分类号
1007 ;
摘要
Introduction: Mitochondria, essential to multicellular life, convert food into ATP to satisfy cellular energy demands. Since different tissues have different energy requirements, mitochondrial density is high in tissues with high metabolic needs, such as the visual system, which is therefore highly susceptible to limited energy supply as a result of mitochondrial dysfunction. Areas covered: Vision impairment is a common feature of most mitochondrial diseases. At the same time, there is mounting evidence that mitochondrial impairment contributes to the pathogenesis of major eye diseases such as glaucoma and might also be involved in the reported vision impairment in neurodegenerative disorders such as Alzheimer's disease. Expert opinion: Rather than relying on symptomatic treatment, acknowledging the mitochondrial origin of visual disorders in mitochondrial, neurodegenerative and ocular diseases could lead to novel therapeutics that aim to modulate mitochondrial function in order to protect against vision loss. This approach has already shown some promising clinical results in inherited retinal disorders, which supports the idea that targeting mitochondria could also be a treatment option for other optic neuropathies.
引用
收藏
页码:721 / 736
页数:16
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