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Medical bioremediation of age-related diseases
Catabolic insufficiency in humans leads to the gradual accumulation of a number of pathogenic compounds associated with age-related diseases, including atherosclerosis, Alzheimer's disease, and macular degeneration. Removal of these compounds is a widely researched therapeutic option, but the u...
Autores principales: | , , , |
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Formato: | Texto |
Lenguaje: | English |
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BioMed Central
2009
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Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2674406/ https://www.ncbi.nlm.nih.gov/pubmed/19358742 http://dx.doi.org/10.1186/1475-2859-8-21 |
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author | Mathieu, Jacques M Schloendorn, John Rittmann, Bruce E Alvarez, Pedro JJ |
author_facet | Mathieu, Jacques M Schloendorn, John Rittmann, Bruce E Alvarez, Pedro JJ |
author_sort | Mathieu, Jacques M |
collection | PubMed |
description | Catabolic insufficiency in humans leads to the gradual accumulation of a number of pathogenic compounds associated with age-related diseases, including atherosclerosis, Alzheimer's disease, and macular degeneration. Removal of these compounds is a widely researched therapeutic option, but the use of antibodies and endogenous human enzymes has failed to produce effective treatments, and may pose risks to cellular homeostasis. Another alternative is "medical bioremediation," the use of microbial enzymes to augment missing catabolic functions. The microbial genetic diversity in most natural environments provides a resource that can be mined for enzymes capable of degrading just about any energy-rich organic compound. This review discusses targets for biodegradation, the identification of candidate microbial enzymes, and enzyme-delivery methods. |
format | Text |
id | pubmed-2674406 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2009 |
publisher | BioMed Central |
record_format | MEDLINE/PubMed |
spelling | pubmed-26744062009-04-29 Medical bioremediation of age-related diseases Mathieu, Jacques M Schloendorn, John Rittmann, Bruce E Alvarez, Pedro JJ Microb Cell Fact Review Catabolic insufficiency in humans leads to the gradual accumulation of a number of pathogenic compounds associated with age-related diseases, including atherosclerosis, Alzheimer's disease, and macular degeneration. Removal of these compounds is a widely researched therapeutic option, but the use of antibodies and endogenous human enzymes has failed to produce effective treatments, and may pose risks to cellular homeostasis. Another alternative is "medical bioremediation," the use of microbial enzymes to augment missing catabolic functions. The microbial genetic diversity in most natural environments provides a resource that can be mined for enzymes capable of degrading just about any energy-rich organic compound. This review discusses targets for biodegradation, the identification of candidate microbial enzymes, and enzyme-delivery methods. BioMed Central 2009-04-09 /pmc/articles/PMC2674406/ /pubmed/19358742 http://dx.doi.org/10.1186/1475-2859-8-21 Text en Copyright © 2009 Mathieu et al; licensee BioMed Central Ltd. http://creativecommons.org/licenses/by/2.0 This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( (http://creativecommons.org/licenses/by/2.0) ), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Review Mathieu, Jacques M Schloendorn, John Rittmann, Bruce E Alvarez, Pedro JJ Medical bioremediation of age-related diseases |
title | Medical bioremediation of age-related diseases |
title_full | Medical bioremediation of age-related diseases |
title_fullStr | Medical bioremediation of age-related diseases |
title_full_unstemmed | Medical bioremediation of age-related diseases |
title_short | Medical bioremediation of age-related diseases |
title_sort | medical bioremediation of age-related diseases |
topic | Review |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2674406/ https://www.ncbi.nlm.nih.gov/pubmed/19358742 http://dx.doi.org/10.1186/1475-2859-8-21 |
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