ArticleInternational journal of molecular sciences2013
Mitochondrial and nuclear DNA damage and repair in age-related macular degeneration.
Article in International journal of molecular sciences, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 59 papers.
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Who cites it
59 citing papers in PubMed, 98 citations in OpenAlex.
- Mitochondrial Dysfunction in the Cardiovascular Disease Continuum: Problems of Studying the Progression During the Follow-Up of the Pathologies.International journal of molecular sciences · 2025Review
- Cardiovascular comorbidities are risk factors for increased oxidative stress and DNA damage in migraine patients: a prospective cohort study.Journal of translational medicine · 2025Article
- Phlorizin Protects Against Oxidative Stress and Inflammation in Age-Related Macular Degeneration Model.Biomolecules · 2025Article
- The Ercc1Aging cell · 2025Article
- Lysosome-Mitochondrial Crosstalk in Cellular Stress and Disease.Antioxidants (Basel, Switzerland) · 2025Review
- IL-17A mediates inflammation-related retinal pigment epithelial cells injuryInternational journal of ophthalmology · 2025Article
- Short-term outcomes of intravitreal faricimab for refractory neovascular age-related macular degeneration.Graefe's archive for clinical and experimental ophthalmology = Albrecht von Graefes Archiv fur klinische und experimentelle Ophthalmologie · 2024Article
- Article
- Potential application of traditional Chinese medicine in age-related macular degeneration-focusing on mitophagy.Frontiers in pharmacology · 2024Review
- Targeting shared pathways in tauopathies and age-related macular degeneration: implications for novel therapies.Frontiers in aging neuroscience · 2024Review
- Stages, pathogenesis, clinical management and advancements in therapies of age-related macular degeneration.International ophthalmology · 2023Review
- Oxidative Stress and Antioxidants in Age-Related Macular Degeneration.Antioxidants (Basel, Switzerland) · 2023Review
- Antioxidative Role of Heterophagy, Autophagy, and Mitophagy in the Retina and Their Association with the Age-Related Macular Degeneration (AMD) Etiopathogenesis.Antioxidants (Basel, Switzerland) · 2023Review
- The Role of Retinal Pigment Epithelial Cells in Age-Related Macular Degeneration: Phagocytosis and Autophagy.Biomolecules · 2023Review
- Dysfunctional Autophagy, Proteostasis, and Mitochondria as a Prelude to Age-Related Macular Degeneration.International journal of molecular sciences · 2023Review
- DNA Damage and Repair in Eye Diseases.International journal of molecular sciences · 2023Review
- Mitochondrial Transplantation Moderately Ameliorates Retinal Degeneration in Royal College of Surgeons Rats.Biomedicines · 2022Article
- Melatonin inhibits NaIOCell & bioscience · 2022Article
- Photobiology of lipofuscin granules in the retinal pigment epithelium cells of the eye: norm, pathology, age.Biophysical reviews · 2022Review
- Arbutin Protects Retinal Pigment Epithelium Against Oxidative Stress by Modulating SIRT1/FOXO3a/PGC-1α/β Pathway.Frontiers in genetics · 2022Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Aging and oxidative stress seem to be the most important factors in the pathogenesis of age-related macular degeneration (AMD), a condition affecting many elderly people in the developed world. However, aging is associated with the accumulation of oxidative damage in many biomolecules, including DNA. Furthermore, mitochondria may be especially important in this process because the reactive oxygen species produced in their electron transport chain can damage cellular components. Therefore, the cellular response to DNA damage, expressed mainly through DNA repair, may play an important role in AMD etiology. In several studies the increase in mitochondrial DNA (mtDNA) damage and mutations, and the decrease in the efficacy of DNA repair have been correlated with the occurrence and the stage of AMD. It has also been shown that mitochondrial DNA accumulates more DNA lesions than nuclear DNA in AMD. However, the DNA damage response in mitochondria is executed by nucleus-encoded proteins, and thus mutagenesis in nuclear DNA (nDNA) may affect the ability to respond to mutagenesis in its mitochondrial counterpart. We reported that lymphocytes from AMD patients displayed a higher amount of total endogenous basal and oxidative DNA damage, exhibited a higher sensitivity to hydrogen peroxide and UV radiation, and repaired the lesions induced by these factors less effectively than did cells from control individuals. We postulate that poor efficacy of DNA repair (i.e., is impaired above average for a particular age) when combined with the enhanced sensitivity of retinal pigment epithelium cells to environmental stress factors, contributes to the pathogenesis of AMD. Collectively, these data suggest that the cellular response to both mitochondrial and nuclear DNA damage may play an important role in AMD pathogenesis.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.