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The Possible Role of Tumor Necrosis Factor-α in Diabetic Polyneuropathy
In this review, the authors provide evidences that imply the role of tumor necrosis factor-α (TNF-α) in the pathogenesis of diabetic complications, especially diabetic polyneuropathy. Under chronic hyperglycemia, endogenous TNF-α production is accelerated in microvascular and neural tissues, which m...
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Formato: | Texto |
Lenguaje: | English |
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Hindawi Publishing Corporation
2003
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Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2478597/ https://www.ncbi.nlm.nih.gov/pubmed/14630568 http://dx.doi.org/10.1155/EDR.2003.65 |
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author | Satoh, Jo Yagihashi, Soroku Toyota, Takayoshi |
author_facet | Satoh, Jo Yagihashi, Soroku Toyota, Takayoshi |
author_sort | Satoh, Jo |
collection | PubMed |
description | In this review, the authors provide evidences that imply the role of tumor necrosis factor-α (TNF-α) in the pathogenesis of diabetic complications, especially diabetic polyneuropathy. Under chronic hyperglycemia, endogenous TNF-α production is accelerated in microvascular and neural tissues, which may undergo an increased microvascular permeability, hypercoagulability, and nerve damage, thus initiating and promoting the development of characteristic lesions of diabetic microangiopathy and polyneuropathy. Enhanced TNF-α production may also promote atherosclerosis due to increased insulin resistance and the expression of adhesion molecules. Clinical application of specific agents that suppress production and/or activity of TNF-α may inhibit the development and exacerbation of chronic diabetic complications. |
format | Text |
id | pubmed-2478597 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2003 |
publisher | Hindawi Publishing Corporation |
record_format | MEDLINE/PubMed |
spelling | pubmed-24785972008-08-18 The Possible Role of Tumor Necrosis Factor-α in Diabetic Polyneuropathy Satoh, Jo Yagihashi, Soroku Toyota, Takayoshi Exp Diabesity Res Research Article In this review, the authors provide evidences that imply the role of tumor necrosis factor-α (TNF-α) in the pathogenesis of diabetic complications, especially diabetic polyneuropathy. Under chronic hyperglycemia, endogenous TNF-α production is accelerated in microvascular and neural tissues, which may undergo an increased microvascular permeability, hypercoagulability, and nerve damage, thus initiating and promoting the development of characteristic lesions of diabetic microangiopathy and polyneuropathy. Enhanced TNF-α production may also promote atherosclerosis due to increased insulin resistance and the expression of adhesion molecules. Clinical application of specific agents that suppress production and/or activity of TNF-α may inhibit the development and exacerbation of chronic diabetic complications. Hindawi Publishing Corporation 2003 /pmc/articles/PMC2478597/ /pubmed/14630568 http://dx.doi.org/10.1155/EDR.2003.65 Text en Copyright © 2003 Hindawi Publishing Corporation. http://creativecommons.org/licenses/by/ 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 | Research Article Satoh, Jo Yagihashi, Soroku Toyota, Takayoshi The Possible Role of Tumor Necrosis Factor-α in Diabetic Polyneuropathy |
title | The Possible Role of Tumor Necrosis Factor-α in Diabetic Polyneuropathy |
title_full | The Possible Role of Tumor Necrosis Factor-α in Diabetic Polyneuropathy |
title_fullStr | The Possible Role of Tumor Necrosis Factor-α in Diabetic Polyneuropathy |
title_full_unstemmed | The Possible Role of Tumor Necrosis Factor-α in Diabetic Polyneuropathy |
title_short | The Possible Role of Tumor Necrosis Factor-α in Diabetic Polyneuropathy |
title_sort | possible role of tumor necrosis factor-α in diabetic polyneuropathy |
topic | Research Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2478597/ https://www.ncbi.nlm.nih.gov/pubmed/14630568 http://dx.doi.org/10.1155/EDR.2003.65 |
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