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Review
. 2011 Dec;36(12):1069-77.
doi: 10.3109/02713683.2011.607536. Epub 2011 Oct 6.

Mitochondrial dysfunction in retinal diseases

Megha Barot  1 , Mitan R Gokulgandhi, Ashim K Mitra
Affiliations
Review

Mitochondrial dysfunction in retinal diseases

Megha Barot et al. Curr Eye Res. 2011 Dec.

Abstract

The mitochondrion is a vital intracellular organelle for retinal cell function and survival. There is growing confirmation to support an association between mitochondrial dysfunction and a number of retinal degenerations. Investigations have also unveiled mitochondrial genomic instability as one of the contributing factors for age-related retinal pathophysiology. This review highlights the role of mitochondrial dysfunction originating from oxidative stress in the etiology of retinal diseases including diabetic retinopathy, glaucoma and age-related macular degeneration (AMD). Moreover, mitochondrial DNA (mtDNA) damage associated with AMD due to susceptibility of mtDNA to oxidative damage and failure of mtDNA repair pathways is also highlighted in this review. The susceptibility of neural retina and retinal pigment epithelium (RPE) mitochondria to oxidative damage with ageing appears to be a major factor in retinal degeneration. It thus appears that the mitochondrion is a weak link in the antioxidant defenses of retinal cells. In addition, failure of mtDNA repair pathways can also specifically contribute towards pathogenesis of AMD. This review will further summarize the prospective role of mitochondria targeting therapeutic agents for the treatment of retinal disease. Mitochondria based drug targeting to diminish oxidative stress or promote repair of mtDNA damage may offer potential alternatives for the treatment of various retinal degenerative diseases.

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Conflict of interest statement

Declaration of interest: The authors report no conflicts of interest.

Figures

FIGURE 1
FIGURE 1
Hyperglycemia mediated mitochondrial dysfunctioning in diabetic retinopathy.
FIGURE 2
FIGURE 2
Involvement of mitochondrial dysfunctioning in glaucoma pathogenesis.
FIGURE 3
FIGURE 3
ROS-induced mtDNA damage based model for development of AMD (1,5,66).
FIGURE 4
FIGURE 4
Strategies for targeted delivery of drugs to Mitochondria.
See this image and copyright information in PMC

References

    1. Jarrett SG, Lin H, Godley BF, Boulton ME. Mitochondrial DNA damage and its potential role in retinal degeneration. Prog Retin Eye Res. 2008;27:596–607. - PubMed
    1. Druzhyna NM, Wilson GL, LeDoux SP. Mitochondrial DNA repair in aging and disease. Mech Ageing Dev. 2008;129:383–390. - PMC - PubMed
    1. Golden TR, Melov S. Mitochondrial DNA mutations, oxidative stress, and aging. Mech Ageing Dev. 2001;122:1577–1589. - PubMed
    1. Sastre J, Pallardó FV, Viña J. Mitochondrial oxidative stress plays a key role in aging and apoptosis. IUBMB Life. 2000;49:427–435. - PubMed
    1. Liang FQ, Godley BF. Oxidative stress-induced mitochondrial DNA damage in human retinal pigment epithelial cells: a possible mechanism for RPE aging and age-related macular degeneration. Exp Eye Res. 2003;76:397–403. - PubMed

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