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Hyperglycemia and Endothelial Dysfunction in Atherosclerosis: Lessons from Type 1 Diabetes

A clear relationship between diabetes and cardiovascular disease has been established for decades. Despite this, the mechanisms by which diabetes contributes to plaque formation remain in question. Some of this confusion derives from studies in type 2 diabetics where multiple components of metabolic...

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Detalles Bibliográficos
Autores principales: Funk, Steven Daniel, Yurdagul, Arif, Orr, A. Wayne
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Hindawi Publishing Corporation 2012
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3303762/
https://www.ncbi.nlm.nih.gov/pubmed/22489274
http://dx.doi.org/10.1155/2012/569654
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author Funk, Steven Daniel
Yurdagul, Arif
Orr, A. Wayne
author_facet Funk, Steven Daniel
Yurdagul, Arif
Orr, A. Wayne
author_sort Funk, Steven Daniel
collection PubMed
description A clear relationship between diabetes and cardiovascular disease has been established for decades. Despite this, the mechanisms by which diabetes contributes to plaque formation remain in question. Some of this confusion derives from studies in type 2 diabetics where multiple components of metabolic syndrome show proatherosclerotic effects independent of underlying diabetes. However, the hyperglycemia that defines the diabetic condition independently affects atherogenesis in cell culture systems, animal models, and human patients. Endothelial cell biology plays a central role in atherosclerotic plaque formation regulating vessel permeability, inflammation, and thrombosis. The current paper highlights the mechanisms by which hyperglycemia affects endothelial cell biology to promote plaque formation.
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spelling pubmed-33037622012-04-09 Hyperglycemia and Endothelial Dysfunction in Atherosclerosis: Lessons from Type 1 Diabetes Funk, Steven Daniel Yurdagul, Arif Orr, A. Wayne Int J Vasc Med Review Article A clear relationship between diabetes and cardiovascular disease has been established for decades. Despite this, the mechanisms by which diabetes contributes to plaque formation remain in question. Some of this confusion derives from studies in type 2 diabetics where multiple components of metabolic syndrome show proatherosclerotic effects independent of underlying diabetes. However, the hyperglycemia that defines the diabetic condition independently affects atherogenesis in cell culture systems, animal models, and human patients. Endothelial cell biology plays a central role in atherosclerotic plaque formation regulating vessel permeability, inflammation, and thrombosis. The current paper highlights the mechanisms by which hyperglycemia affects endothelial cell biology to promote plaque formation. Hindawi Publishing Corporation 2012 2012-02-14 /pmc/articles/PMC3303762/ /pubmed/22489274 http://dx.doi.org/10.1155/2012/569654 Text en Copyright © 2012 Steven Daniel Funk et al. https://creativecommons.org/licenses/by/3.0/ This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Review Article
Funk, Steven Daniel
Yurdagul, Arif
Orr, A. Wayne
Hyperglycemia and Endothelial Dysfunction in Atherosclerosis: Lessons from Type 1 Diabetes
title Hyperglycemia and Endothelial Dysfunction in Atherosclerosis: Lessons from Type 1 Diabetes
title_full Hyperglycemia and Endothelial Dysfunction in Atherosclerosis: Lessons from Type 1 Diabetes
title_fullStr Hyperglycemia and Endothelial Dysfunction in Atherosclerosis: Lessons from Type 1 Diabetes
title_full_unstemmed Hyperglycemia and Endothelial Dysfunction in Atherosclerosis: Lessons from Type 1 Diabetes
title_short Hyperglycemia and Endothelial Dysfunction in Atherosclerosis: Lessons from Type 1 Diabetes
title_sort hyperglycemia and endothelial dysfunction in atherosclerosis: lessons from type 1 diabetes
topic Review Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3303762/
https://www.ncbi.nlm.nih.gov/pubmed/22489274
http://dx.doi.org/10.1155/2012/569654
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