Abstract
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.
Highlights
Reactive oxygen species (ROS), including free radicals, play important roles in cellular signaling, being an important element of organismal homeostasis [1]
In this review we showed that mitochondria might be a serious, if not the most serious, source of reactive oxygen species (ROS) playing a major role in Age-related macular degeneration (AMD) pathogenesis
At least two hypotheses supporting the central role of mitochondrial reactive oxygen species (mtROS) and damage to mitochondrial DNA (mtDNA) in AMD pathogenesis can be considered (Figure 3)
Summary
Reactive oxygen species (ROS), including free radicals, play important roles in cellular signaling, being an important element of organismal homeostasis [1]. 2019, 20, 2374 source of elevated levels of ROS and, most importantly, the exact association between oxidative effects occurring in RPE and the onset and progression of AMD still need explanation [33]. We present arguments that mitochondrial dysfunction underlined by damage to mitochondrial DNA (mtDNA) may be the reason for increased ROS production in RPE associated with AMD onset and progression. This concept is not entirely new, but we present certain novel arguments and update some previous data
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