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Hydrogen Sulfide and Endoplasmic Reticulum Stress: A Potential Therapeutic Target for Central Nervous System Degeneration Diseases
There are three members of the endogenous gas transmitter family. The first two are nitric oxide and carbon monoxide, and the third newly added member is hydrogen sulfide (H(2)S). They all have similar functions: relaxing blood vessels, smoothing muscles, and getting involved in the regulation of ne...
Autores principales: | , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
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Frontiers Media S.A.
2020
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Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7240010/ https://www.ncbi.nlm.nih.gov/pubmed/32477150 http://dx.doi.org/10.3389/fphar.2020.00702 |
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author | Zhong, Huimin Yu, Huan Chen, Junjue Sun, Jun Guo, Lei Huang, Ping Zhong, Yisheng |
author_facet | Zhong, Huimin Yu, Huan Chen, Junjue Sun, Jun Guo, Lei Huang, Ping Zhong, Yisheng |
author_sort | Zhong, Huimin |
collection | PubMed |
description | There are three members of the endogenous gas transmitter family. The first two are nitric oxide and carbon monoxide, and the third newly added member is hydrogen sulfide (H(2)S). They all have similar functions: relaxing blood vessels, smoothing muscles, and getting involved in the regulation of neuronal excitation, learning, and memory. The cystathionine β-synthase (CBS), 3-mercaptopyruvate sulfur transferase acts together with cysteine aminotransferase (3-MST/CAT), cystathionine γ-lyase (CSE), and 3-mercaptopyruvate sulfur transferase with D-amino acid oxidase (3-MST/DAO) pathways are involved in the enzymatic production of H(2)S. More and more researches focus on the role of H(2)S in the central nervous system (CNS), and H(2)S plays a significant function in neuroprotection processes, regulating the function of the nervous system as a signaling molecule in the CNS. Endoplasmic reticulum stress (ERS) and protein misfolding in its mechanism are related to neurodegenerative diseases. H(2)S exhibits a wide variety of cytoprotective and physiological functions in the CNS degenerative diseases by regulating ERS. This review summarized on the neuroprotective effect of H(2)S for ERS played in several CNS diseases including Alzheimer’s disease, Parkinson’s disease, and depression disorder, and discussed the corresponding possible signaling pathways or mechanisms as well. |
format | Online Article Text |
id | pubmed-7240010 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2020 |
publisher | Frontiers Media S.A. |
record_format | MEDLINE/PubMed |
spelling | pubmed-72400102020-05-29 Hydrogen Sulfide and Endoplasmic Reticulum Stress: A Potential Therapeutic Target for Central Nervous System Degeneration Diseases Zhong, Huimin Yu, Huan Chen, Junjue Sun, Jun Guo, Lei Huang, Ping Zhong, Yisheng Front Pharmacol Pharmacology There are three members of the endogenous gas transmitter family. The first two are nitric oxide and carbon monoxide, and the third newly added member is hydrogen sulfide (H(2)S). They all have similar functions: relaxing blood vessels, smoothing muscles, and getting involved in the regulation of neuronal excitation, learning, and memory. The cystathionine β-synthase (CBS), 3-mercaptopyruvate sulfur transferase acts together with cysteine aminotransferase (3-MST/CAT), cystathionine γ-lyase (CSE), and 3-mercaptopyruvate sulfur transferase with D-amino acid oxidase (3-MST/DAO) pathways are involved in the enzymatic production of H(2)S. More and more researches focus on the role of H(2)S in the central nervous system (CNS), and H(2)S plays a significant function in neuroprotection processes, regulating the function of the nervous system as a signaling molecule in the CNS. Endoplasmic reticulum stress (ERS) and protein misfolding in its mechanism are related to neurodegenerative diseases. H(2)S exhibits a wide variety of cytoprotective and physiological functions in the CNS degenerative diseases by regulating ERS. This review summarized on the neuroprotective effect of H(2)S for ERS played in several CNS diseases including Alzheimer’s disease, Parkinson’s disease, and depression disorder, and discussed the corresponding possible signaling pathways or mechanisms as well. Frontiers Media S.A. 2020-05-14 /pmc/articles/PMC7240010/ /pubmed/32477150 http://dx.doi.org/10.3389/fphar.2020.00702 Text en Copyright © 2020 Zhong, Yu, Chen, Sun, Guo, Huang and Zhong http://creativecommons.org/licenses/by/4.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms. |
spellingShingle | Pharmacology Zhong, Huimin Yu, Huan Chen, Junjue Sun, Jun Guo, Lei Huang, Ping Zhong, Yisheng Hydrogen Sulfide and Endoplasmic Reticulum Stress: A Potential Therapeutic Target for Central Nervous System Degeneration Diseases |
title | Hydrogen Sulfide and Endoplasmic Reticulum Stress: A Potential Therapeutic Target for Central Nervous System Degeneration Diseases |
title_full | Hydrogen Sulfide and Endoplasmic Reticulum Stress: A Potential Therapeutic Target for Central Nervous System Degeneration Diseases |
title_fullStr | Hydrogen Sulfide and Endoplasmic Reticulum Stress: A Potential Therapeutic Target for Central Nervous System Degeneration Diseases |
title_full_unstemmed | Hydrogen Sulfide and Endoplasmic Reticulum Stress: A Potential Therapeutic Target for Central Nervous System Degeneration Diseases |
title_short | Hydrogen Sulfide and Endoplasmic Reticulum Stress: A Potential Therapeutic Target for Central Nervous System Degeneration Diseases |
title_sort | hydrogen sulfide and endoplasmic reticulum stress: a potential therapeutic target for central nervous system degeneration diseases |
topic | Pharmacology |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7240010/ https://www.ncbi.nlm.nih.gov/pubmed/32477150 http://dx.doi.org/10.3389/fphar.2020.00702 |
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