ReviewInternational journal of molecular sciences2012
Genetic variability in DNA repair proteins in age-related macular degeneration.
Review in International journal of molecular sciences, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers, 1 of them a synthesis that pooled it.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
16 citing papers in PubMed, 1 synthesis or guideline pooled it, 28 citations in OpenAlex.
- Genetic polymorphisms in ERCC1 and ERCC2 genes are associated with response to chemotherapy in osteosarcoma patients among Chinese population: a meta-analysis.World journal of surgical oncology · 2017Pooled it
- Polymorphisms in Base Excision Repair Genes and Association with Multiple Sclerosis in a Pilot Study on a Central European Population.International journal of molecular sciences · 2025Article
- Construction of an Exudative Age-Related Macular Degeneration Diagnostic and Therapeutic Molecular Network Using Multi-Layer Network Analysis, a Fuzzy Logic Model, and Deep Learning Techniques: Are Retinal and Brain Neurodegenerative Disorders Related?Pharmaceuticals (Basel, Switzerland) · 2023Article
- Genetic Aspects of Age-Related Macular Degeneration and Their Therapeutic Potential.International journal of molecular sciences · 2022Review
- Review
- Microvascular contributions to age-related macular degeneration (AMD): from mechanisms of choriocapillaris aging to novel interventions.GeroScience · 2019Review
- PGC-1α Protects RPE Cells of the Aging Retina against Oxidative Stress-Induced Degeneration through the Regulation of Senescence and Mitochondrial Quality Control. The Significance for AMD Pathogenesis.International journal of molecular sciences · 2018Review
- Photosensitization of A2E triggers telomere dysfunction and accelerates retinal pigment epithelium senescence.Cell death & disease · 2018Article
- Autophagy regulates death of retinal pigment epithelium cells in age-related macular degeneration.Cell biology and toxicology · 2017Review
- Risk factors and biomarkers of age-related macular degeneration.Progress in retinal and eye research · 2016Review
- In-depth analyses unveil the association and possible functional involvement of novel RAD51B polymorphisms in age-related macular degeneration.Age (Dordrecht, Netherlands) · 2014Article
- Aging is not a disease: distinguishing age-related macular degeneration from aging.Progress in retinal and eye research · 2013Review
- The significance of the alteration of 8-OHdG in serous ovarian carcinoma.Journal of ovarian research · 2013Article
- Mitochondrial and nuclear DNA damage and repair in age-related macular degeneration.International journal of molecular sciences · 2013Article
- Association between age-related macular degeneration and 25(OH) vitamin D levels in the Turkish population.Arquivos brasileiros de oftalmologiaArticle
- Melatonin in Retinal Physiology and Pathology: The Case of Age-Related Macular Degeneration.Oxidative medicine and cellular longevityReview
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The pathogenesis of age-related macular degeneration (AMD) is complex and involves interactions between environmental and genetic factors, with oxidative stress playing an important role inducing damage in biomolecules, including DNA. Therefore, genetic variability in the components of DNA repair systems may influence the ability of the cell to cope with oxidative stress and in this way contribute to the pathogenesis of AMD. However, few reports have been published on this subject so far. We demonstrated that the c.977C>G polymorphism (rs1052133) in the hOGG1 gene and the c.972G>C polymorphism (rs3219489) in the MUTYH gene, the products of which play important roles in the repair of oxidatively damaged DNA, might be associated with the risk of AMD. Oxidative stress may promote misincorporation of uracil into DNA, where it is targeted by several DNA glycosylases. We observed that the g.4235T>C (rs2337395) and c.-32A>G (rs3087404) polymorphisms in two genes encoding such glycosylases, UNG and SMUG1, respectively, could be associated with the occurrence of AMD. Polymorphisms in some other DNA repair genes, including XPD (ERCC2), XRCC1 and ERCC6 (CSB) have also been reported to be associated with AMD. These data confirm the importance of the cellular reaction to DNA damage, and this may be influenced by variability in DNA repair genes, 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.