IMR Press / FBL / Volume 16 / Issue 4 / DOI: 10.2741/3789

Frontiers in Bioscience-Landmark (FBL) is published by IMR Press from Volume 26 Issue 5 (2021). Previous articles were published by another publisher on a subscription basis, and they are hosted by IMR Press on imrpress.com as a courtesy and upon agreement with Frontiers in Bioscience.

Open Access Article
DNA damage and repair in age-related macular degeneration
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1 Department of Molecular Genetics, University of Lodz, Banacha 12/16, 90-237 Lodz, Poland
2 Department of Ophthalmology, Medical University of Warsaw and Samodzielny Szpital Okulistyczny, Sierakowskiego 13, 03-709 Warsaw, Poland

Academic Editor: Kai Kaarniranta

Front. Biosci. (Landmark Ed) 2011, 16(4), 1291–1301; https://doi.org/10.2741/3789
Published: 1 January 2011
(This article belongs to the Special Issue Pathogenetic mechanism of age-related macular degeneration)
Abstract

Oxidative stress may play an important role in the pathogenesis of age-related macular degeneration (AMD). Mitochondria produce reactive oxygen species (ROS), which induce degenerative changes typical for AMD. Mitochondrial DNA (mtDNA) is targeted by ROS and it is considered to be more vulnerable to damage than nuclear DNA (nDNA) due to the impaired DNA repair system, lack of nucleosomal organization and close vicinity of mitochondrial oxidative chain. Some reports suggest the association between mtDNA damage and AMD. However, the metabolism of mtDNA is mainly determined by the expression of nDNA. Therefore, the extent of damage to mtDNA in retinal cells depends on the overall efficacy of nDNA repair, which decreases with age. We showed an association between nDNA damage and repair and AMD. Also well-recognized factors of AMD pathogenesis, age and smoking, may exert their effects through the DNA damage and repair. In conclusion, DNA damage and repair, both in mitochondrial and nuclear genome, may play an important role in the pathogenesis of AMD, and their mutual relationship in this disease needs further study.

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