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Advanced Glycation End-Products and Diabetic Neuropathy of the Retina
Diabetic retinopathy is a tissue-specific neurovascular impairment of the retina in patients with both type 1 and type 2 diabetes. Several pathological factors are involved in the progressive impairment of the interdependence between cells that consist of the neurovascular units (NVUs). The advanced...
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Formato: | Online Artículo Texto |
Lenguaje: | English |
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MDPI
2023
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Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9917392/ https://www.ncbi.nlm.nih.gov/pubmed/36769249 http://dx.doi.org/10.3390/ijms24032927 |
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author | Oshitari, Toshiyuki |
author_facet | Oshitari, Toshiyuki |
author_sort | Oshitari, Toshiyuki |
collection | PubMed |
description | Diabetic retinopathy is a tissue-specific neurovascular impairment of the retina in patients with both type 1 and type 2 diabetes. Several pathological factors are involved in the progressive impairment of the interdependence between cells that consist of the neurovascular units (NVUs). The advanced glycation end-products (AGEs) are one of the major pathological factors that cause the impairments of neurovascular coupling in diabetic retinopathy. Although the exact mechanisms for the toxicities of the AGEs in diabetic retinopathy have not been definitively determined, the AGE-receptor of the AGE (RAGE) axis, production of reactive oxygen species, inflammatory reactions, and the activation of the cell death pathways are associated with the impairment of the NVUs in diabetic retinopathy. More specifically, neuronal cell death is an irreversible change that is directly associated with vision reduction in diabetic patients. Thus, neuroprotective therapies must be established for diabetic retinopathy. The AGEs are one of the therapeutic targets to examine to ameliorate the pathological changes in the NVUs in diabetic retinopathy. This review focuses on the basic and pathological findings of AGE-induced neurovascular abnormalities and the potential therapeutic approaches, including the use of anti-glycated drugs to protect the AGE-induced impairments of the NVUs in diabetic retinopathy. |
format | Online Article Text |
id | pubmed-9917392 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2023 |
publisher | MDPI |
record_format | MEDLINE/PubMed |
spelling | pubmed-99173922023-02-11 Advanced Glycation End-Products and Diabetic Neuropathy of the Retina Oshitari, Toshiyuki Int J Mol Sci Review Diabetic retinopathy is a tissue-specific neurovascular impairment of the retina in patients with both type 1 and type 2 diabetes. Several pathological factors are involved in the progressive impairment of the interdependence between cells that consist of the neurovascular units (NVUs). The advanced glycation end-products (AGEs) are one of the major pathological factors that cause the impairments of neurovascular coupling in diabetic retinopathy. Although the exact mechanisms for the toxicities of the AGEs in diabetic retinopathy have not been definitively determined, the AGE-receptor of the AGE (RAGE) axis, production of reactive oxygen species, inflammatory reactions, and the activation of the cell death pathways are associated with the impairment of the NVUs in diabetic retinopathy. More specifically, neuronal cell death is an irreversible change that is directly associated with vision reduction in diabetic patients. Thus, neuroprotective therapies must be established for diabetic retinopathy. The AGEs are one of the therapeutic targets to examine to ameliorate the pathological changes in the NVUs in diabetic retinopathy. This review focuses on the basic and pathological findings of AGE-induced neurovascular abnormalities and the potential therapeutic approaches, including the use of anti-glycated drugs to protect the AGE-induced impairments of the NVUs in diabetic retinopathy. MDPI 2023-02-02 /pmc/articles/PMC9917392/ /pubmed/36769249 http://dx.doi.org/10.3390/ijms24032927 Text en © 2023 by the author. https://creativecommons.org/licenses/by/4.0/Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/). |
spellingShingle | Review Oshitari, Toshiyuki Advanced Glycation End-Products and Diabetic Neuropathy of the Retina |
title | Advanced Glycation End-Products and Diabetic Neuropathy of the Retina |
title_full | Advanced Glycation End-Products and Diabetic Neuropathy of the Retina |
title_fullStr | Advanced Glycation End-Products and Diabetic Neuropathy of the Retina |
title_full_unstemmed | Advanced Glycation End-Products and Diabetic Neuropathy of the Retina |
title_short | Advanced Glycation End-Products and Diabetic Neuropathy of the Retina |
title_sort | advanced glycation end-products and diabetic neuropathy of the retina |
topic | Review |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9917392/ https://www.ncbi.nlm.nih.gov/pubmed/36769249 http://dx.doi.org/10.3390/ijms24032927 |
work_keys_str_mv | AT oshitaritoshiyuki advancedglycationendproductsanddiabeticneuropathyoftheretina |