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Mitochondrial DNA Damage in Age-Related Macular Degeneration

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Posted 24 May 2019 - 10:22 AM

One of the early features of age-related macular degeneration, in which the retina degenerates, causing progressive blindness, is a rising level of oxidative stress in the retinal pigment epithelium. Researchers here consider a role for mitochondrial DNA damage in the generation of this oxidative damage. Mitochondria are the power plants of the cell, descendants of ancient symbiotic bacteria that still retain a little of their original DNA. They carry out energetic chemical operations that result in a flow of oxidative molecules as a by-product. Damage to mitochondrial DNA that causes loss of proteins essential to the molecular machinery inside a mitochondrion can lead to a sizable leap in production of oxidative molecules, not just by mitochondria, but exported by the cell into the surrounding tissue.

Age-related macular degeneration (AMD) is a complex eye disease that affects millions of people worldwide and is the main reason for legal blindness and vision loss in the elderly in developed countries. Although the cause of AMD pathogenesis is not known, oxidative stress-related damage to retinal pigment epithelium (RPE) is considered an early event in AMD induction. However, the precise cause of such damage and of the induction of oxidative stress, including related oxidative effects occurring in RPE and the onset and progression of AMD, are not well understood.

Many results point to mitochondria as a source of elevated levels of reactive oxygen species (ROS) in AMD. This ROS increase can be associated with aging and effects induced by other AMD risk factors and is correlated with damage to mitochondrial DNA. Therefore, mitochondrial DNA (mtDNA) damage can be an essential element of AMD pathogenesis. This is supported by many studies that show a greater susceptibility of mtDNA than nuclear DNA to DNA-damaging agents in AMD. Therefore, the mitochondrial DNA damage reaction (mtDDR) is important in AMD prevention and in slowing down its progression as is ROS-targeting AMD therapy. However, we know far less about mtDNA than its nuclear counterparts. Further research should measure DNA damage in order to compare it in mitochondria and the nucleus, as current methods have serious disadvantages.

Link: https://doi.org/10.3390/ijms20102374

View the full article at FightAging

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