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MiR-22 as a metabolic silencer and liver tumor suppressor
With obesity rate consistently increasing, a strong relationship between obesity and fatty liver disease has been discovered. More than 90% of bariatric surgery patients also have non-alcoholic fatty liver diseases (NAFLDs). NAFLD and non-alcoholic steatohepatitis (NASH), which are the hepatic manif...
Autores principales: | , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
2020
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7523703/ https://www.ncbi.nlm.nih.gov/pubmed/33005474 http://dx.doi.org/10.1016/j.livres.2020.06.001 |
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author | Wang, Lijun Wang, Yu-Shiuan Mugiyanto, Eko Chang, Wei-Chiao Yvonne Wan, Yu-Jui |
author_facet | Wang, Lijun Wang, Yu-Shiuan Mugiyanto, Eko Chang, Wei-Chiao Yvonne Wan, Yu-Jui |
author_sort | Wang, Lijun |
collection | PubMed |
description | With obesity rate consistently increasing, a strong relationship between obesity and fatty liver disease has been discovered. More than 90% of bariatric surgery patients also have non-alcoholic fatty liver diseases (NAFLDs). NAFLD and non-alcoholic steatohepatitis (NASH), which are the hepatic manifestations of metabolic syndrome, can lead to liver carcinogenesis. Unfortunately, there is no effective medicine that can be used to treat NASH or liver cancer. Thus, it is critically important to understand the mechanism underlying the development of these diseases. Extensive evidence suggests that microRNA 22 (miR-22) can be a diagnostic marker for liver diseases as well as a treatment target. This review paper focuses on the roles of miR-22 in metabolism, steatosis, and liver carcinogenesis. Literature search is limited based on the publications included in the PubMed database in the recent 10 years. |
format | Online Article Text |
id | pubmed-7523703 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2020 |
record_format | MEDLINE/PubMed |
spelling | pubmed-75237032021-06-01 MiR-22 as a metabolic silencer and liver tumor suppressor Wang, Lijun Wang, Yu-Shiuan Mugiyanto, Eko Chang, Wei-Chiao Yvonne Wan, Yu-Jui Liver Res Article With obesity rate consistently increasing, a strong relationship between obesity and fatty liver disease has been discovered. More than 90% of bariatric surgery patients also have non-alcoholic fatty liver diseases (NAFLDs). NAFLD and non-alcoholic steatohepatitis (NASH), which are the hepatic manifestations of metabolic syndrome, can lead to liver carcinogenesis. Unfortunately, there is no effective medicine that can be used to treat NASH or liver cancer. Thus, it is critically important to understand the mechanism underlying the development of these diseases. Extensive evidence suggests that microRNA 22 (miR-22) can be a diagnostic marker for liver diseases as well as a treatment target. This review paper focuses on the roles of miR-22 in metabolism, steatosis, and liver carcinogenesis. Literature search is limited based on the publications included in the PubMed database in the recent 10 years. 2020-06-09 2020-06 /pmc/articles/PMC7523703/ /pubmed/33005474 http://dx.doi.org/10.1016/j.livres.2020.06.001 Text en This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/). |
spellingShingle | Article Wang, Lijun Wang, Yu-Shiuan Mugiyanto, Eko Chang, Wei-Chiao Yvonne Wan, Yu-Jui MiR-22 as a metabolic silencer and liver tumor suppressor |
title | MiR-22 as a metabolic silencer and liver tumor suppressor |
title_full | MiR-22 as a metabolic silencer and liver tumor suppressor |
title_fullStr | MiR-22 as a metabolic silencer and liver tumor suppressor |
title_full_unstemmed | MiR-22 as a metabolic silencer and liver tumor suppressor |
title_short | MiR-22 as a metabolic silencer and liver tumor suppressor |
title_sort | mir-22 as a metabolic silencer and liver tumor suppressor |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7523703/ https://www.ncbi.nlm.nih.gov/pubmed/33005474 http://dx.doi.org/10.1016/j.livres.2020.06.001 |
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