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Role of Hydrogen Sulfide in Ischemia-Reperfusion Injury
Ischemia-reperfusion (I/R) injury is one of the major causes of high morbidity, disability, and mortality in the world. I/R injury remains a complicated and unresolved situation in clinical practice, especially in the field of solid organ transplantation. Hydrogen sulfide (H(2)S) is the third gaseou...
Autores principales: | , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Hindawi Publishing Corporation
2015
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4443900/ https://www.ncbi.nlm.nih.gov/pubmed/26064416 http://dx.doi.org/10.1155/2015/186908 |
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author | Wu, Dongdong Wang, Jun Li, Hui Xue, Mengzhou Ji, Ailing Li, Yanzhang |
author_facet | Wu, Dongdong Wang, Jun Li, Hui Xue, Mengzhou Ji, Ailing Li, Yanzhang |
author_sort | Wu, Dongdong |
collection | PubMed |
description | Ischemia-reperfusion (I/R) injury is one of the major causes of high morbidity, disability, and mortality in the world. I/R injury remains a complicated and unresolved situation in clinical practice, especially in the field of solid organ transplantation. Hydrogen sulfide (H(2)S) is the third gaseous signaling molecule and plays a broad range of physiological and pathophysiological roles in mammals. H(2)S could protect against I/R injury in many organs and tissues, such as heart, liver, kidney, brain, intestine, stomach, hind-limb, lung, and retina. The goal of this review is to highlight recent findings regarding the role of H(2)S in I/R injury. In this review, we present the production and metabolism of H(2)S and further discuss the effect and mechanism of H(2)S in I/R injury. |
format | Online Article Text |
id | pubmed-4443900 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2015 |
publisher | Hindawi Publishing Corporation |
record_format | MEDLINE/PubMed |
spelling | pubmed-44439002015-06-10 Role of Hydrogen Sulfide in Ischemia-Reperfusion Injury Wu, Dongdong Wang, Jun Li, Hui Xue, Mengzhou Ji, Ailing Li, Yanzhang Oxid Med Cell Longev Review Article Ischemia-reperfusion (I/R) injury is one of the major causes of high morbidity, disability, and mortality in the world. I/R injury remains a complicated and unresolved situation in clinical practice, especially in the field of solid organ transplantation. Hydrogen sulfide (H(2)S) is the third gaseous signaling molecule and plays a broad range of physiological and pathophysiological roles in mammals. H(2)S could protect against I/R injury in many organs and tissues, such as heart, liver, kidney, brain, intestine, stomach, hind-limb, lung, and retina. The goal of this review is to highlight recent findings regarding the role of H(2)S in I/R injury. In this review, we present the production and metabolism of H(2)S and further discuss the effect and mechanism of H(2)S in I/R injury. Hindawi Publishing Corporation 2015 2015-05-12 /pmc/articles/PMC4443900/ /pubmed/26064416 http://dx.doi.org/10.1155/2015/186908 Text en Copyright © 2015 Dongdong Wu et al. 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 Wu, Dongdong Wang, Jun Li, Hui Xue, Mengzhou Ji, Ailing Li, Yanzhang Role of Hydrogen Sulfide in Ischemia-Reperfusion Injury |
title | Role of Hydrogen Sulfide in Ischemia-Reperfusion Injury |
title_full | Role of Hydrogen Sulfide in Ischemia-Reperfusion Injury |
title_fullStr | Role of Hydrogen Sulfide in Ischemia-Reperfusion Injury |
title_full_unstemmed | Role of Hydrogen Sulfide in Ischemia-Reperfusion Injury |
title_short | Role of Hydrogen Sulfide in Ischemia-Reperfusion Injury |
title_sort | role of hydrogen sulfide in ischemia-reperfusion injury |
topic | Review Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4443900/ https://www.ncbi.nlm.nih.gov/pubmed/26064416 http://dx.doi.org/10.1155/2015/186908 |
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