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Role of advanced glycation end products in cellular signaling()
Improvements in health care and lifestyle have led to an elevated lifespan and increased focus on age-associated diseases, such as neurodegeneration, cardiovascular disease, frailty and arteriosclerosis. In all these chronic diseases protein, lipid or nucleic acid modifications are involved, includi...
Autores principales: | , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Elsevier
2014
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3949097/ https://www.ncbi.nlm.nih.gov/pubmed/24624331 http://dx.doi.org/10.1016/j.redox.2013.12.016 |
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author | Ott, Christiane Jacobs, Kathleen Haucke, Elisa Navarrete Santos, Anne Grune, Tilman Simm, Andreas |
author_facet | Ott, Christiane Jacobs, Kathleen Haucke, Elisa Navarrete Santos, Anne Grune, Tilman Simm, Andreas |
author_sort | Ott, Christiane |
collection | PubMed |
description | Improvements in health care and lifestyle have led to an elevated lifespan and increased focus on age-associated diseases, such as neurodegeneration, cardiovascular disease, frailty and arteriosclerosis. In all these chronic diseases protein, lipid or nucleic acid modifications are involved, including cross-linked and non-degradable aggregates, such as advanced glycation end products (AGEs). Formation of endogenous or uptake of dietary AGEs can lead to further protein modifications and activation of several inflammatory signaling pathways. This review will give an overview of the most prominent AGE-mediated signaling cascades, AGE receptor interactions, prevention of AGE formation and the impact of AGEs during pathophysiological processes. |
format | Online Article Text |
id | pubmed-3949097 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2014 |
publisher | Elsevier |
record_format | MEDLINE/PubMed |
spelling | pubmed-39490972014-03-12 Role of advanced glycation end products in cellular signaling() Ott, Christiane Jacobs, Kathleen Haucke, Elisa Navarrete Santos, Anne Grune, Tilman Simm, Andreas Redox Biol Review Article Improvements in health care and lifestyle have led to an elevated lifespan and increased focus on age-associated diseases, such as neurodegeneration, cardiovascular disease, frailty and arteriosclerosis. In all these chronic diseases protein, lipid or nucleic acid modifications are involved, including cross-linked and non-degradable aggregates, such as advanced glycation end products (AGEs). Formation of endogenous or uptake of dietary AGEs can lead to further protein modifications and activation of several inflammatory signaling pathways. This review will give an overview of the most prominent AGE-mediated signaling cascades, AGE receptor interactions, prevention of AGE formation and the impact of AGEs during pathophysiological processes. Elsevier 2014-01-09 /pmc/articles/PMC3949097/ /pubmed/24624331 http://dx.doi.org/10.1016/j.redox.2013.12.016 Text en © 2014 The Authors https://creativecommons.org/licenses/by-nc-sa/3.0/This work is licensed under a Creative Commons Attribution-NonCommercial-ShareAlike 3.0 Unported License (https://creativecommons.org/licenses/by-nc-sa/3.0/) . |
spellingShingle | Review Article Ott, Christiane Jacobs, Kathleen Haucke, Elisa Navarrete Santos, Anne Grune, Tilman Simm, Andreas Role of advanced glycation end products in cellular signaling() |
title | Role of advanced glycation end products in cellular signaling() |
title_full | Role of advanced glycation end products in cellular signaling() |
title_fullStr | Role of advanced glycation end products in cellular signaling() |
title_full_unstemmed | Role of advanced glycation end products in cellular signaling() |
title_short | Role of advanced glycation end products in cellular signaling() |
title_sort | role of advanced glycation end products in cellular signaling() |
topic | Review Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3949097/ https://www.ncbi.nlm.nih.gov/pubmed/24624331 http://dx.doi.org/10.1016/j.redox.2013.12.016 |
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