Fibroblast growth factor 21 potentially inhibits microRNA-33 expression to affect macrophage actions

Atherosclerosis is a chronic inflammatory disease with complex pathological processes. MicroRNA-33 (miR-33), a novel non-coding RNA that coexpresses with sterol regulatory element-binding proteins (SREBPs), affects macrophage actions to prevent atherosclerosis. Fibroblast growth factor 21 (FGF21) is...

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Detalles Bibliográficos
Autores principales: Guo, Yuan, Luo, Fei, Yi, Yuhong, Xu, Danyan
Formato: Online Artículo Texto
Lenguaje:English
Publicado: BioMed Central 2016
Materias:
Hypothesis
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5134291/
https://www.ncbi.nlm.nih.gov/pubmed/27905947
http://dx.doi.org/10.1186/s12944-016-0381-6
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author Guo, Yuan
Luo, Fei
Yi, Yuhong
Xu, Danyan
author_facet Guo, Yuan
Luo, Fei
Yi, Yuhong
Xu, Danyan
author_sort Guo, Yuan
collection PubMed
description Atherosclerosis is a chronic inflammatory disease with complex pathological processes. MicroRNA-33 (miR-33), a novel non-coding RNA that coexpresses with sterol regulatory element-binding proteins (SREBPs), affects macrophage actions to prevent atherosclerosis. Fibroblast growth factor 21 (FGF21) is an important regulator of lipid metabolism, especially for macrophage-related cholesterol export, but the mechanism is not fully studied. Interestingly, FGF21 has been evidenced to prevent atherosclerosis via inhibiting SREBP-2 expression. Therefore, we speculate that FGF21 may be a potential regulator for miR-33 with an aim of insight into novel anti-atherosclerotic mechanisms and research fields.
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spelling pubmed-51342912016-12-15 Fibroblast growth factor 21 potentially inhibits microRNA-33 expression to affect macrophage actions Guo, Yuan Luo, Fei Yi, Yuhong Xu, Danyan Lipids Health Dis Hypothesis Atherosclerosis is a chronic inflammatory disease with complex pathological processes. MicroRNA-33 (miR-33), a novel non-coding RNA that coexpresses with sterol regulatory element-binding proteins (SREBPs), affects macrophage actions to prevent atherosclerosis. Fibroblast growth factor 21 (FGF21) is an important regulator of lipid metabolism, especially for macrophage-related cholesterol export, but the mechanism is not fully studied. Interestingly, FGF21 has been evidenced to prevent atherosclerosis via inhibiting SREBP-2 expression. Therefore, we speculate that FGF21 may be a potential regulator for miR-33 with an aim of insight into novel anti-atherosclerotic mechanisms and research fields. BioMed Central 2016-12-01 /pmc/articles/PMC5134291/ /pubmed/27905947 http://dx.doi.org/10.1186/s12944-016-0381-6 Text en © The Author(s). 2016 Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.
spellingShingle Hypothesis
Guo, Yuan
Luo, Fei
Yi, Yuhong
Xu, Danyan
Fibroblast growth factor 21 potentially inhibits microRNA-33 expression to affect macrophage actions
title Fibroblast growth factor 21 potentially inhibits microRNA-33 expression to affect macrophage actions
title_full Fibroblast growth factor 21 potentially inhibits microRNA-33 expression to affect macrophage actions
title_fullStr Fibroblast growth factor 21 potentially inhibits microRNA-33 expression to affect macrophage actions
title_full_unstemmed Fibroblast growth factor 21 potentially inhibits microRNA-33 expression to affect macrophage actions
title_short Fibroblast growth factor 21 potentially inhibits microRNA-33 expression to affect macrophage actions
title_sort fibroblast growth factor 21 potentially inhibits microrna-33 expression to affect macrophage actions
topic Hypothesis
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5134291/
https://www.ncbi.nlm.nih.gov/pubmed/27905947
http://dx.doi.org/10.1186/s12944-016-0381-6
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AT luofei fibroblastgrowthfactor21potentiallyinhibitsmicrorna33expressiontoaffectmacrophageactions
AT yiyuhong fibroblastgrowthfactor21potentiallyinhibitsmicrorna33expressiontoaffectmacrophageactions
AT xudanyan fibroblastgrowthfactor21potentiallyinhibitsmicrorna33expressiontoaffectmacrophageactions

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