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What is Known Regarding the Participation of Factor Nrf-2 in Liver Regeneration?
It has been known for years that, after chemical damage or surgical removal of its tissue, the liver initiates a series of changes that, taken together, are known as regeneration, which are focused on the recovery of lost or affected tissue in terms of the anatomical or functional aspect. The Nuclea...
Autores principales: | , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
MDPI
2015
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4493454/ https://www.ncbi.nlm.nih.gov/pubmed/26010752 http://dx.doi.org/10.3390/cells4020169 |
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author | Morales-González, José A. Madrigal-Santillán, Eduardo Morales-González, Ángel Bautista, Mirandeli Gayosso-Islas, Evila Sánchez-Moreno, Cecilia |
author_facet | Morales-González, José A. Madrigal-Santillán, Eduardo Morales-González, Ángel Bautista, Mirandeli Gayosso-Islas, Evila Sánchez-Moreno, Cecilia |
author_sort | Morales-González, José A. |
collection | PubMed |
description | It has been known for years that, after chemical damage or surgical removal of its tissue, the liver initiates a series of changes that, taken together, are known as regeneration, which are focused on the recovery of lost or affected tissue in terms of the anatomical or functional aspect. The Nuclear factor-erythroid 2-related factor (Nrf-2) is a reduction-oxidation reaction (redox)-sensitive transcriptional factor, with the basic leucine Zipper domain (bZIP) motif, encoding the NFE2L2 gene. The Keap1-Nrf2-ARE pathway is transcendental in the regulation of various cellular processes, such as antioxidant defenses, redox equilibrium, the inflammatory process, the apoptotic processes, intermediate metabolism, detoxification, and cellular proliferation. Some reports have demonstrated the regulator role of Nrf-2 in the cellular cycle of the hepatocyte, as well as in the modulation of the antioxidant response and of apoptotic processes during liver regeneration. It has been reported that there is a delay in liver regeneration after Partial hepatectomy (PH) in the absence of Nrf-2, and similarly as a regulator of hepatic cytoprotection due to diverse chemical or biological agents, and in diseases such as hepatitis, fibrosis, cirrhosis, and liver cancer. This regulator/protector capacity is due to the modulation of the Antioxidant response elements (ARE). It is postulated that oxidative stress (OS) can participate in the initial stages of liver regeneration and that Nrf-2 can probably participate. Studies are lacking on the different initiation stages, maintenance, and the termination of liver regeneration alone or with ethanol. |
format | Online Article Text |
id | pubmed-4493454 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2015 |
publisher | MDPI |
record_format | MEDLINE/PubMed |
spelling | pubmed-44934542015-07-07 What is Known Regarding the Participation of Factor Nrf-2 in Liver Regeneration? Morales-González, José A. Madrigal-Santillán, Eduardo Morales-González, Ángel Bautista, Mirandeli Gayosso-Islas, Evila Sánchez-Moreno, Cecilia Cells Review It has been known for years that, after chemical damage or surgical removal of its tissue, the liver initiates a series of changes that, taken together, are known as regeneration, which are focused on the recovery of lost or affected tissue in terms of the anatomical or functional aspect. The Nuclear factor-erythroid 2-related factor (Nrf-2) is a reduction-oxidation reaction (redox)-sensitive transcriptional factor, with the basic leucine Zipper domain (bZIP) motif, encoding the NFE2L2 gene. The Keap1-Nrf2-ARE pathway is transcendental in the regulation of various cellular processes, such as antioxidant defenses, redox equilibrium, the inflammatory process, the apoptotic processes, intermediate metabolism, detoxification, and cellular proliferation. Some reports have demonstrated the regulator role of Nrf-2 in the cellular cycle of the hepatocyte, as well as in the modulation of the antioxidant response and of apoptotic processes during liver regeneration. It has been reported that there is a delay in liver regeneration after Partial hepatectomy (PH) in the absence of Nrf-2, and similarly as a regulator of hepatic cytoprotection due to diverse chemical or biological agents, and in diseases such as hepatitis, fibrosis, cirrhosis, and liver cancer. This regulator/protector capacity is due to the modulation of the Antioxidant response elements (ARE). It is postulated that oxidative stress (OS) can participate in the initial stages of liver regeneration and that Nrf-2 can probably participate. Studies are lacking on the different initiation stages, maintenance, and the termination of liver regeneration alone or with ethanol. MDPI 2015-05-20 /pmc/articles/PMC4493454/ /pubmed/26010752 http://dx.doi.org/10.3390/cells4020169 Text en © 2015 by the authors; licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution license (http://creativecommons.org/licenses/by/4.0/). |
spellingShingle | Review Morales-González, José A. Madrigal-Santillán, Eduardo Morales-González, Ángel Bautista, Mirandeli Gayosso-Islas, Evila Sánchez-Moreno, Cecilia What is Known Regarding the Participation of Factor Nrf-2 in Liver Regeneration? |
title | What is Known Regarding the Participation of Factor Nrf-2 in Liver Regeneration? |
title_full | What is Known Regarding the Participation of Factor Nrf-2 in Liver Regeneration? |
title_fullStr | What is Known Regarding the Participation of Factor Nrf-2 in Liver Regeneration? |
title_full_unstemmed | What is Known Regarding the Participation of Factor Nrf-2 in Liver Regeneration? |
title_short | What is Known Regarding the Participation of Factor Nrf-2 in Liver Regeneration? |
title_sort | what is known regarding the participation of factor nrf-2 in liver regeneration? |
topic | Review |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4493454/ https://www.ncbi.nlm.nih.gov/pubmed/26010752 http://dx.doi.org/10.3390/cells4020169 |
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