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Role and Possible Mechanisms of Sirt1 in Depression

Depression is a common, devastating illness. Due to complicated causes and limited treatments, depression is still a major problem that plagues the world. Silent information regulator 1 (Sirt1) is a deacetylase at the consumption of NAD(+) and is involved in gene silencing, cell cycle, fat and gluco...

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Detalles Bibliográficos
Autores principales: Lu, Guofang, Li, Jianguo, Zhang, Hongmei, Zhao, Xin, Yan, Liang-Jun, Yang, Xiaorong
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Hindawi 2018
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5831942/
https://www.ncbi.nlm.nih.gov/pubmed/29643977
http://dx.doi.org/10.1155/2018/8596903
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author Lu, Guofang
Li, Jianguo
Zhang, Hongmei
Zhao, Xin
Yan, Liang-Jun
Yang, Xiaorong
author_facet Lu, Guofang
Li, Jianguo
Zhang, Hongmei
Zhao, Xin
Yan, Liang-Jun
Yang, Xiaorong
author_sort Lu, Guofang
collection PubMed
description Depression is a common, devastating illness. Due to complicated causes and limited treatments, depression is still a major problem that plagues the world. Silent information regulator 1 (Sirt1) is a deacetylase at the consumption of NAD(+) and is involved in gene silencing, cell cycle, fat and glucose metabolism, cellular oxidative stress, and senescence. Sirt1 has now become a critical therapeutic target for a number of diseases. Recently, a genetic study has received considerable attention for depression and found that Sirt1 is a potential gene target. In this short review article, we attempt to present an up-to-date knowledge of depression and Sirt1 of the sirtuin family, describe the different effects of Sirt1 on depression, and further discuss possible mechanisms of Sirt1 including glial activation, neurogenesis, circadian control, and potential signaling molecules. Thus, it will open a new avenue for clinical treatment of depression.
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spelling pubmed-58319422018-04-11 Role and Possible Mechanisms of Sirt1 in Depression Lu, Guofang Li, Jianguo Zhang, Hongmei Zhao, Xin Yan, Liang-Jun Yang, Xiaorong Oxid Med Cell Longev Review Article Depression is a common, devastating illness. Due to complicated causes and limited treatments, depression is still a major problem that plagues the world. Silent information regulator 1 (Sirt1) is a deacetylase at the consumption of NAD(+) and is involved in gene silencing, cell cycle, fat and glucose metabolism, cellular oxidative stress, and senescence. Sirt1 has now become a critical therapeutic target for a number of diseases. Recently, a genetic study has received considerable attention for depression and found that Sirt1 is a potential gene target. In this short review article, we attempt to present an up-to-date knowledge of depression and Sirt1 of the sirtuin family, describe the different effects of Sirt1 on depression, and further discuss possible mechanisms of Sirt1 including glial activation, neurogenesis, circadian control, and potential signaling molecules. Thus, it will open a new avenue for clinical treatment of depression. Hindawi 2018-01-31 /pmc/articles/PMC5831942/ /pubmed/29643977 http://dx.doi.org/10.1155/2018/8596903 Text en Copyright © 2018 Guofang Lu et al. http://creativecommons.org/licenses/by/4.0/ 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
Lu, Guofang
Li, Jianguo
Zhang, Hongmei
Zhao, Xin
Yan, Liang-Jun
Yang, Xiaorong
Role and Possible Mechanisms of Sirt1 in Depression
title Role and Possible Mechanisms of Sirt1 in Depression
title_full Role and Possible Mechanisms of Sirt1 in Depression
title_fullStr Role and Possible Mechanisms of Sirt1 in Depression
title_full_unstemmed Role and Possible Mechanisms of Sirt1 in Depression
title_short Role and Possible Mechanisms of Sirt1 in Depression
title_sort role and possible mechanisms of sirt1 in depression
topic Review Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5831942/
https://www.ncbi.nlm.nih.gov/pubmed/29643977
http://dx.doi.org/10.1155/2018/8596903
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