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The PI3K/Akt pathway: a critical player in intervertebral disc degeneration

Intervertebral disc degeneration (IDD) is thought to be the primary cause of low back pain, a severe public health problem worldwide. Current therapy for IDD aims to alleviate the symptoms and does not target the underlying pathological alternations within the disc. Activation of the phosphatidylino...

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Autores principales: Ouyang, Zhi-Hua, Wang, Wen-Jun, Yan, Yi-Guo, Wang, Bing, Lv, Guo-Hua
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Impact Journals LLC 2017
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5593690/
https://www.ncbi.nlm.nih.gov/pubmed/28915718
http://dx.doi.org/10.18632/oncotarget.18628
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author Ouyang, Zhi-Hua
Wang, Wen-Jun
Yan, Yi-Guo
Wang, Bing
Lv, Guo-Hua
author_facet Ouyang, Zhi-Hua
Wang, Wen-Jun
Yan, Yi-Guo
Wang, Bing
Lv, Guo-Hua
author_sort Ouyang, Zhi-Hua
collection PubMed
description Intervertebral disc degeneration (IDD) is thought to be the primary cause of low back pain, a severe public health problem worldwide. Current therapy for IDD aims to alleviate the symptoms and does not target the underlying pathological alternations within the disc. Activation of the phosphatidylinositol 3-kinase (PI3K)/Akt pathway protects against IDD, which is attributed to increase of ECM content, prevention of cell apoptosis, facilitation of cell proliferation, induction or prevention of cell autophagy, alleviation of oxidative damage, and adaptation of hypoxic microenvironment. In the current review, we summarize recent progression on activation and negative regulation of the PI3K/Akt signaling pathway, and highlight its impact on IDD. Targeting this pathway could become an attractive therapeutic strategy for IDD in the near future.
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spelling pubmed-55936902017-09-14 The PI3K/Akt pathway: a critical player in intervertebral disc degeneration Ouyang, Zhi-Hua Wang, Wen-Jun Yan, Yi-Guo Wang, Bing Lv, Guo-Hua Oncotarget Review Intervertebral disc degeneration (IDD) is thought to be the primary cause of low back pain, a severe public health problem worldwide. Current therapy for IDD aims to alleviate the symptoms and does not target the underlying pathological alternations within the disc. Activation of the phosphatidylinositol 3-kinase (PI3K)/Akt pathway protects against IDD, which is attributed to increase of ECM content, prevention of cell apoptosis, facilitation of cell proliferation, induction or prevention of cell autophagy, alleviation of oxidative damage, and adaptation of hypoxic microenvironment. In the current review, we summarize recent progression on activation and negative regulation of the PI3K/Akt signaling pathway, and highlight its impact on IDD. Targeting this pathway could become an attractive therapeutic strategy for IDD in the near future. Impact Journals LLC 2017-06-27 /pmc/articles/PMC5593690/ /pubmed/28915718 http://dx.doi.org/10.18632/oncotarget.18628 Text en Copyright: © 2017 Ouyang et al. http://creativecommons.org/licenses/by/3.0/ This article is distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/3.0/) (CC-BY), which permits unrestricted use and redistribution provided that the original author and source are credited.
spellingShingle Review
Ouyang, Zhi-Hua
Wang, Wen-Jun
Yan, Yi-Guo
Wang, Bing
Lv, Guo-Hua
The PI3K/Akt pathway: a critical player in intervertebral disc degeneration
title The PI3K/Akt pathway: a critical player in intervertebral disc degeneration
title_full The PI3K/Akt pathway: a critical player in intervertebral disc degeneration
title_fullStr The PI3K/Akt pathway: a critical player in intervertebral disc degeneration
title_full_unstemmed The PI3K/Akt pathway: a critical player in intervertebral disc degeneration
title_short The PI3K/Akt pathway: a critical player in intervertebral disc degeneration
title_sort pi3k/akt pathway: a critical player in intervertebral disc degeneration
topic Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5593690/
https://www.ncbi.nlm.nih.gov/pubmed/28915718
http://dx.doi.org/10.18632/oncotarget.18628
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