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Regulation of Lipid Metabolism by Lamin in Mutation-Related Diseases
Nuclear lamins, known as type 5 intermediate fibers, are composed of lamin A, lamin C, lamin B1, and lamin B2, which are encoded by LMNA and LMNB genes, respectively. Importantly, mutations in nuclear lamins not only participate in lipid disorders but also in the human diseases, such as lipodystroph...
Autores principales: | , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Frontiers Media S.A.
2022
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8914069/ https://www.ncbi.nlm.nih.gov/pubmed/35281936 http://dx.doi.org/10.3389/fphar.2022.820857 |
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author | Peng, Yue Tang, Qianyu Xiao, Fan Fu, Nian |
author_facet | Peng, Yue Tang, Qianyu Xiao, Fan Fu, Nian |
author_sort | Peng, Yue |
collection | PubMed |
description | Nuclear lamins, known as type 5 intermediate fibers, are composed of lamin A, lamin C, lamin B1, and lamin B2, which are encoded by LMNA and LMNB genes, respectively. Importantly, mutations in nuclear lamins not only participate in lipid disorders but also in the human diseases, such as lipodystrophy, metabolic-associated fatty liver disease, and dilated cardiomyopathy. Among those diseases, the mechanism of lamin has been widely discussed. Thereby, this review mainly focuses on the regulatory mechanism of the mutations in the lamin gene in lipid alterations and the human diseases. Considering the protean actions, targeting nuclear lamins may be a potent therapeutic avenue for lipid metabolic disorders and human diseases in the future. |
format | Online Article Text |
id | pubmed-8914069 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2022 |
publisher | Frontiers Media S.A. |
record_format | MEDLINE/PubMed |
spelling | pubmed-89140692022-03-12 Regulation of Lipid Metabolism by Lamin in Mutation-Related Diseases Peng, Yue Tang, Qianyu Xiao, Fan Fu, Nian Front Pharmacol Pharmacology Nuclear lamins, known as type 5 intermediate fibers, are composed of lamin A, lamin C, lamin B1, and lamin B2, which are encoded by LMNA and LMNB genes, respectively. Importantly, mutations in nuclear lamins not only participate in lipid disorders but also in the human diseases, such as lipodystrophy, metabolic-associated fatty liver disease, and dilated cardiomyopathy. Among those diseases, the mechanism of lamin has been widely discussed. Thereby, this review mainly focuses on the regulatory mechanism of the mutations in the lamin gene in lipid alterations and the human diseases. Considering the protean actions, targeting nuclear lamins may be a potent therapeutic avenue for lipid metabolic disorders and human diseases in the future. Frontiers Media S.A. 2022-02-25 /pmc/articles/PMC8914069/ /pubmed/35281936 http://dx.doi.org/10.3389/fphar.2022.820857 Text en Copyright © 2022 Peng, Tang, Xiao and Fu. https://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 Peng, Yue Tang, Qianyu Xiao, Fan Fu, Nian Regulation of Lipid Metabolism by Lamin in Mutation-Related Diseases |
title | Regulation of Lipid Metabolism by Lamin in Mutation-Related Diseases |
title_full | Regulation of Lipid Metabolism by Lamin in Mutation-Related Diseases |
title_fullStr | Regulation of Lipid Metabolism by Lamin in Mutation-Related Diseases |
title_full_unstemmed | Regulation of Lipid Metabolism by Lamin in Mutation-Related Diseases |
title_short | Regulation of Lipid Metabolism by Lamin in Mutation-Related Diseases |
title_sort | regulation of lipid metabolism by lamin in mutation-related diseases |
topic | Pharmacology |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8914069/ https://www.ncbi.nlm.nih.gov/pubmed/35281936 http://dx.doi.org/10.3389/fphar.2022.820857 |
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