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Signaling Mechanisms in the Regulation of Renal Matrix Metabolism in Diabetes
Renal hypertrophy and accumulation of extracellular matrix proteins are among cardinal manifestations of diabetic nephropathy. TGF beta system has been implicated in the pathogenesis of these manifestations. Among signaling pathways activated in the kidney in diabetes, mTOR- (mammalian target of rap...
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Formato: | Online Artículo Texto |
Lenguaje: | English |
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Hindawi Publishing Corporation
2012
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Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3290898/ https://www.ncbi.nlm.nih.gov/pubmed/22454628 http://dx.doi.org/10.1155/2012/749812 |
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author | Mariappan, Meenalakshmi M. |
author_facet | Mariappan, Meenalakshmi M. |
author_sort | Mariappan, Meenalakshmi M. |
collection | PubMed |
description | Renal hypertrophy and accumulation of extracellular matrix proteins are among cardinal manifestations of diabetic nephropathy. TGF beta system has been implicated in the pathogenesis of these manifestations. Among signaling pathways activated in the kidney in diabetes, mTOR- (mammalian target of rapamycin-)regulated pathways are pivotal in orchestrating high glucose-induced production of ECM proteins leading to functional and structural changes in the kidney culminating in adverse outcomes. Understanding signaling pathways that influence individual matrix protein expression could lead to the development of new interventional strategies. This paper will highlight some of the diverse components of the signaling network stimulated by hyperglycemia with an emphasis on extracellular matrix protein metabolism in the kidney in diabetes. |
format | Online Article Text |
id | pubmed-3290898 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2012 |
publisher | Hindawi Publishing Corporation |
record_format | MEDLINE/PubMed |
spelling | pubmed-32908982012-03-27 Signaling Mechanisms in the Regulation of Renal Matrix Metabolism in Diabetes Mariappan, Meenalakshmi M. Exp Diabetes Res Review Article Renal hypertrophy and accumulation of extracellular matrix proteins are among cardinal manifestations of diabetic nephropathy. TGF beta system has been implicated in the pathogenesis of these manifestations. Among signaling pathways activated in the kidney in diabetes, mTOR- (mammalian target of rapamycin-)regulated pathways are pivotal in orchestrating high glucose-induced production of ECM proteins leading to functional and structural changes in the kidney culminating in adverse outcomes. Understanding signaling pathways that influence individual matrix protein expression could lead to the development of new interventional strategies. This paper will highlight some of the diverse components of the signaling network stimulated by hyperglycemia with an emphasis on extracellular matrix protein metabolism in the kidney in diabetes. Hindawi Publishing Corporation 2012 2012-02-19 /pmc/articles/PMC3290898/ /pubmed/22454628 http://dx.doi.org/10.1155/2012/749812 Text en Copyright © 2012 Meenalakshmi M. Mariappan. 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 Mariappan, Meenalakshmi M. Signaling Mechanisms in the Regulation of Renal Matrix Metabolism in Diabetes |
title | Signaling Mechanisms in the Regulation of Renal Matrix Metabolism in Diabetes |
title_full | Signaling Mechanisms in the Regulation of Renal Matrix Metabolism in Diabetes |
title_fullStr | Signaling Mechanisms in the Regulation of Renal Matrix Metabolism in Diabetes |
title_full_unstemmed | Signaling Mechanisms in the Regulation of Renal Matrix Metabolism in Diabetes |
title_short | Signaling Mechanisms in the Regulation of Renal Matrix Metabolism in Diabetes |
title_sort | signaling mechanisms in the regulation of renal matrix metabolism in diabetes |
topic | Review Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3290898/ https://www.ncbi.nlm.nih.gov/pubmed/22454628 http://dx.doi.org/10.1155/2012/749812 |
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