Abstract:
:The similarities between glaucoma and mitochondrial optic neuropathies have driven a growing interest in exploring mitochondrial function in glaucoma. The specific loss of retinal ganglion cells is a common feature of mitochondrial diseases - not only the classic mitochondrial optic neuropathies of Leber's Hereditary Optic Neuropathy and Autosomal Dominant Optic Atrophy - but also occurring together with more severe central nervous system involvement in many other syndromic mitochondrial diseases. The retinal ganglion cell, due to peculiar structural and energetic constraints, appears acutely susceptible to mitochondrial dysfunction. Mitochondrial function is also well known to decline with aging in post-mitotic tissues including neurons. Because age is a risk factor for glaucoma this adds another impetus to investigating mitochondria in this common and heterogeneous neurodegenerative disease. Mitochondrial function may be impaired by either nuclear gene or mitochondrial DNA genetic risk factors, by mechanical stress or chronic hypoperfusion consequent to the commonly raised intraocular pressure in glaucomatous eyes, or by toxic xenobiotic or even light-induced oxidative stress. If primary or secondary mitochondrial dysfunction is further established as contributing to glaucoma pathogenesis, emerging therapies aimed at optimizing mitochondrial function represent potentially exciting new clinical treatments that may slow retinal ganglion cell and vision loss in glaucoma.
journal_name
Exp Eye Resjournal_title
Experimental eye researchauthors
Lee S,Van Bergen NJ,Kong GY,Chrysostomou V,Waugh HS,O'Neill EC,Crowston JG,Trounce IAdoi
10.1016/j.exer.2010.07.015subject
Has Abstractpub_date
2011-08-01 00:00:00pages
204-12issue
2eissn
0014-4835issn
1096-0007pii
S0014-4835(10)00226-5journal_volume
93pub_type
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journal_title:Experimental eye research
pub_type: 杂志文章
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更新日期:1997-04-01 00:00:00
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