scholarly journals Allelic interaction effects of DNA damage and repair genes on the predisposition to age-related cataract

PLoS ONE ◽  
2018 ◽  
Vol 13 (4) ◽  
pp. e0184478 ◽  
Author(s):  
Mei Yang ◽  
Junfang Zhang ◽  
Shu Su ◽  
Bai Qin ◽  
Lihua Kang ◽  
...  
Keyword(s):  
Dna Damage ◽  
Interaction Effects ◽  
Dna Damage And Repair ◽  
Age Related ◽  
Allelic Interaction ◽  
Repair Genes

DNA damage and repair in age-related macular degeneration

2009 ◽  
Vol 669 (1-2) ◽  
pp. 169-176 ◽  
Author(s):  
Jacek P. Szaflik ◽  
Katarzyna Janik-Papis ◽  
Ewelina Synowiec ◽  
Dominika Ksiazek ◽  
Magdalena Zaras ◽  
...  
Keyword(s):  
Dna Damage ◽  
Macular Degeneration ◽  
Age Related Macular Degeneration ◽  
Dna Damage And Repair ◽  
Age Related

scholarly journals Mitochondrial and Nuclear DNA Damage and Repair in Age-Related Macular Degeneration

2013 ◽  
Vol 14 (2) ◽  
pp. 2996-3010 ◽  
Author(s):  
Janusz Blasiak ◽  
Sylwester Glowacki ◽  
Anu Kauppinen ◽  
Kai Kaarniranta
Keyword(s):  
Dna Damage ◽  
Macular Degeneration ◽  
Nuclear Dna ◽  
Age Related Macular Degeneration ◽  
Dna Damage And Repair ◽  
Age Related

scholarly journals G Protein-Coupled Receptor Systems as Crucial Regulators of DNA Damage Response Processes

2018 ◽  
Vol 19 (10) ◽  
pp. 2919 ◽  
Author(s):  
Hanne Leysen ◽  
Jaana van Gastel ◽  
Jhana Hendrickx ◽  
Paula Santos-Otte ◽  
Bronwen Martin ◽  
...  
Keyword(s):  
Dna Damage ◽  
G Protein ◽  
Dna Damage Response ◽  
Dna Damage And Repair ◽  
Signaling Systems ◽  
Age Related ◽  
Complex Biological Process ◽  
Damage Response ◽  
G Protein Coupled

G protein-coupled receptors (GPCRs) and their associated proteins represent one of the most diverse cellular signaling systems involved in both physiological and pathophysiological processes. Aging represents perhaps the most complex biological process in humans and involves a progressive degradation of systemic integrity and physiological resilience. This is in part mediated by age-related aberrations in energy metabolism, mitochondrial function, protein folding and sorting, inflammatory activity and genomic stability. Indeed, an increased rate of unrepaired DNA damage is considered to be one of the ‘hallmarks’ of aging. Over the last two decades our appreciation of the complexity of GPCR signaling systems has expanded their functional signaling repertoire. One such example of this is the incipient role of GPCRs and GPCR-interacting proteins in DNA damage and repair mechanisms. Emerging data now suggest that GPCRs could function as stress sensors for intracellular damage, e.g., oxidative stress. Given this role of GPCRs in the DNA damage response process, coupled to the effective history of drug targeting of these receptors, this suggests that one important future activity of GPCR therapeutics is the rational control of DNA damage repair systems.

Oxidative Stress, Ocular Disease and Diabetes Retinopathy

2019 ◽  
Vol 24 (40) ◽  
pp. 4726-4741 ◽  
Author(s):  
Orathai Tangvarasittichai ◽  
Surapon Tangvarasittichai
Keyword(s):  
Oxidative Stress ◽  
Dna Damage ◽  
Cell Death ◽  
Protein Modification ◽  
Morphological Changes ◽  
Corneal Dystrophy ◽  
Age Related Macular Degeneration ◽  
Ocular Diseases ◽  
Retinal Light Damage ◽  
Age Related

Background: Oxidative stress is caused by free radicals or oxidant productions, including lipid peroxidation, protein modification, DNA damage and apoptosis or cell death and results in cellular degeneration and neurodegeneration from damage to macromolecules. Results: Accumulation of the DNA damage (8HOdG) products and the end products of LPO (including aldehyde, diene, triene conjugates and Schiff’s bases) were noted in the research studies. Significantly higher levels of these products in comparison with the controls were observed. Oxidative stress induced changes to ocular cells and tissues. Typical changes include ECM accumulation, cell dysfunction, cell death, advanced senescence, disarrangement or rearrangement of the cytoskeleton and released inflammatory cytokines. It is involved in ocular diseases, including keratoconus, Fuchs endothelial corneal dystrophy, and granular corneal dystrophy type 2, cataract, age-related macular degeneration, primary open-angle glaucoma, retinal light damage, and retinopathy of prematurity. These ocular diseases are the cause of irreversible blindness worldwide. Conclusions: Oxidative stress, inflammation and autophagy are implicated in biochemical and morphological changes in these ocular tissues. The development of therapy is a major target for the management care of these ocular diseases.

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