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Emergent role of gasotransmitters in ischemia-reperfusion injury
Nitric oxide (NO), carbon monoxide (CO) and hydrogen sulfide (H(2)S) are lipid-soluble, endogenously produced gaseous messenger molecules collectively known as gasotransmitters. Over the last several decades, gasotransmitters have emerged as potent cytoprotective mediators in various models of tissu...
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Formato: | Online Artículo Texto |
Lenguaje: | English |
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BioMed Central
2011
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3191488/ https://www.ncbi.nlm.nih.gov/pubmed/22146243 http://dx.doi.org/10.1186/2045-9912-1-3 |
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author | Moody, Bridgette F Calvert, John W |
author_facet | Moody, Bridgette F Calvert, John W |
author_sort | Moody, Bridgette F |
collection | PubMed |
description | Nitric oxide (NO), carbon monoxide (CO) and hydrogen sulfide (H(2)S) are lipid-soluble, endogenously produced gaseous messenger molecules collectively known as gasotransmitters. Over the last several decades, gasotransmitters have emerged as potent cytoprotective mediators in various models of tissue and cellular injury. Specifically, when used at physiological levels, the exogenous and endogenous manipulation of these three gases has been shown to modulate ischemia/reperfusion injury by inducing a number of cytoprotective mechanisms including: induction of vasodilatation, inhibition of apoptosis, modulation of mitochondrial respiration, induction of antioxidants, and inhibition of inflammation. However, while the actions are similar, there are some differences in the mechanisms by which these gasotransmitters induce these effects and the regulatory actions of the enzyme systems can vary depending upon the gas being investigated. Furthermore, there does appear to be some crosstalk between the gases, which can provide synergistic effects and additional regulatory effects. This review article will discuss several models and mechanisms of gas-mediated cytoprotection, as well as provide a brief discussion on the complex interactions between the gasotransmitter systems. |
format | Online Article Text |
id | pubmed-3191488 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2011 |
publisher | BioMed Central |
record_format | MEDLINE/PubMed |
spelling | pubmed-31914882011-12-01 Emergent role of gasotransmitters in ischemia-reperfusion injury Moody, Bridgette F Calvert, John W Med Gas Res Review Nitric oxide (NO), carbon monoxide (CO) and hydrogen sulfide (H(2)S) are lipid-soluble, endogenously produced gaseous messenger molecules collectively known as gasotransmitters. Over the last several decades, gasotransmitters have emerged as potent cytoprotective mediators in various models of tissue and cellular injury. Specifically, when used at physiological levels, the exogenous and endogenous manipulation of these three gases has been shown to modulate ischemia/reperfusion injury by inducing a number of cytoprotective mechanisms including: induction of vasodilatation, inhibition of apoptosis, modulation of mitochondrial respiration, induction of antioxidants, and inhibition of inflammation. However, while the actions are similar, there are some differences in the mechanisms by which these gasotransmitters induce these effects and the regulatory actions of the enzyme systems can vary depending upon the gas being investigated. Furthermore, there does appear to be some crosstalk between the gases, which can provide synergistic effects and additional regulatory effects. This review article will discuss several models and mechanisms of gas-mediated cytoprotection, as well as provide a brief discussion on the complex interactions between the gasotransmitter systems. BioMed Central 2011-04-27 /pmc/articles/PMC3191488/ /pubmed/22146243 http://dx.doi.org/10.1186/2045-9912-1-3 Text en Copyright ©2011 Moody and Calvert; 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 Moody, Bridgette F Calvert, John W Emergent role of gasotransmitters in ischemia-reperfusion injury |
title | Emergent role of gasotransmitters in ischemia-reperfusion injury |
title_full | Emergent role of gasotransmitters in ischemia-reperfusion injury |
title_fullStr | Emergent role of gasotransmitters in ischemia-reperfusion injury |
title_full_unstemmed | Emergent role of gasotransmitters in ischemia-reperfusion injury |
title_short | Emergent role of gasotransmitters in ischemia-reperfusion injury |
title_sort | emergent role of gasotransmitters in ischemia-reperfusion injury |
topic | Review |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3191488/ https://www.ncbi.nlm.nih.gov/pubmed/22146243 http://dx.doi.org/10.1186/2045-9912-1-3 |
work_keys_str_mv | AT moodybridgettef emergentroleofgasotransmittersinischemiareperfusioninjury AT calvertjohnw emergentroleofgasotransmittersinischemiareperfusioninjury |