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Energy metabolism and rheumatic diseases: from cell to organism
In rheumatic and other chronic inflammatory diseases, high amounts of energy for the activated immune system have to be provided and allocated by energy metabolism. In recent time many new insights have been gained into the control of the immune response through metabolic signals. Activation of immu...
Autores principales: | , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
BioMed Central
2012
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3446535/ https://www.ncbi.nlm.nih.gov/pubmed/22747923 http://dx.doi.org/10.1186/ar3885 |
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author | Spies, Cornelia M Straub, Rainer H Buttgereit, Frank |
author_facet | Spies, Cornelia M Straub, Rainer H Buttgereit, Frank |
author_sort | Spies, Cornelia M |
collection | PubMed |
description | In rheumatic and other chronic inflammatory diseases, high amounts of energy for the activated immune system have to be provided and allocated by energy metabolism. In recent time many new insights have been gained into the control of the immune response through metabolic signals. Activation of immune cells as well as reduced nutrient supply and hypoxia in inflamed tissues cause stimulation of glycolysis and other cellular metabolic pathways. However, persistent cellular metabolic signals can promote ongoing chronic inflammation and loss of immune tolerance. On the organism level, the neuroendocrine immune response of the hypothalamic-pituitary adrenal axis and sympathetic nervous system, which is meant to overcome a transient inflammatory episode, can lead to metabolic disease sequelae if chronically activated. We conclude that, on cellular and organism levels, a prolonged energy appeal reaction is an important factor of chronic inflammatory disease etiology. |
format | Online Article Text |
id | pubmed-3446535 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2012 |
publisher | BioMed Central |
record_format | MEDLINE/PubMed |
spelling | pubmed-34465352012-12-29 Energy metabolism and rheumatic diseases: from cell to organism Spies, Cornelia M Straub, Rainer H Buttgereit, Frank Arthritis Res Ther Review In rheumatic and other chronic inflammatory diseases, high amounts of energy for the activated immune system have to be provided and allocated by energy metabolism. In recent time many new insights have been gained into the control of the immune response through metabolic signals. Activation of immune cells as well as reduced nutrient supply and hypoxia in inflamed tissues cause stimulation of glycolysis and other cellular metabolic pathways. However, persistent cellular metabolic signals can promote ongoing chronic inflammation and loss of immune tolerance. On the organism level, the neuroendocrine immune response of the hypothalamic-pituitary adrenal axis and sympathetic nervous system, which is meant to overcome a transient inflammatory episode, can lead to metabolic disease sequelae if chronically activated. We conclude that, on cellular and organism levels, a prolonged energy appeal reaction is an important factor of chronic inflammatory disease etiology. BioMed Central 2012 2012-06-29 /pmc/articles/PMC3446535/ /pubmed/22747923 http://dx.doi.org/10.1186/ar3885 Text en Copyright ©2012 BioMed Central Ltd |
spellingShingle | Review Spies, Cornelia M Straub, Rainer H Buttgereit, Frank Energy metabolism and rheumatic diseases: from cell to organism |
title | Energy metabolism and rheumatic diseases: from cell to organism |
title_full | Energy metabolism and rheumatic diseases: from cell to organism |
title_fullStr | Energy metabolism and rheumatic diseases: from cell to organism |
title_full_unstemmed | Energy metabolism and rheumatic diseases: from cell to organism |
title_short | Energy metabolism and rheumatic diseases: from cell to organism |
title_sort | energy metabolism and rheumatic diseases: from cell to organism |
topic | Review |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3446535/ https://www.ncbi.nlm.nih.gov/pubmed/22747923 http://dx.doi.org/10.1186/ar3885 |
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