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40
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Text
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<a href="http://doi.org/10.1016/j.molmet.2021.101244" target="_blank" rel="noreferrer noopener">http://doi.org/10.1016/j.molmet.2021.101244</a>
Pages
3-11
ISSN
2212-8778
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<a href="http://neomed.idm.oclc.org/login?url=http://doi.org/10.1016/j.molmet.2021.101244" target="_blank" rel="noreferrer noopener">NEOMED Full-text Holding (if available) - Proxy DOI: 10.1016/j.molmet.2021.101244</a>
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Update Year & Number
May 2021 List
NEOMED College
NEOMED College of Medicine
NEOMED Department
Department of Integrative Medical Sciences
NEOMED Postdoc Publications
NEOMED Student Publications
Dublin Core
The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/.
Title
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Hepatocyte miR-34a is a key regulator in the development and progression of non-alcoholic fatty liver disease.
Publisher
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Molecular Metabolism
Date
A point or period of time associated with an event in the lifecycle of the resource
2021
2021-04-27
Subject
The topic of the resource
miR-34a; NAFLD; Lipogenesis; bile acids; Bile acids; lipid absorption; lipogenesis; Lipid absorption
Creator
An entity primarily responsible for making the resource
Xu Y; Zhu Y; Hu S; Pan X; Bawa FC; Wang HH; Wang DQ; Yin L; Zhang Y
Description
An account of the resource
Objectives: Hepatic miR-34a expression is elevated in diet-induced or genetically obese mice, and patients with non-alcoholic steatohepatitis (NASH), yet the role of hepatocyte miR-34a in the progression of non-alcoholic fatty liver disease (NAFLD) from non-alcoholic fatty liver (NAFL) to NASH remains to be elucidated.; Methods: Mice over-expressing or deficient in hepatocyte miR-34a and their control mice were fed a diet enriched in fats, cholesterol and fructose (HFCF) to induce NASH. C57BL/6 mice with NASH were treated with an miR-34a inhibitor or a scramble control oligo. The effect of miR-34a on the development, progression or reversal of NAFLD was determined.; Results: Hepatocyte-specific expression of miR-34a aggravated HFCF diet-induced NAFLD. In contrast, germline or adult-onset loss of hepatocyte miR-34a attenuated the development and progression of NAFLD. In addition, pharmacological inhibition of miR-34a reversed HFCF diet-induced steatohepatitis. Mechanistically, hepatocyte miR-34a regulated the development and progression of NAFLD by inducing lipid absorption, lipogenesis, inflammation and apoptosis, and inhibiting fatty acid oxidation.; Conclusions: Hepatocyte miR-34a is an important regulator in the development and progression of NAFLD. MiR-34a may be a useful target for treating NAFLD. (Copyright © 2021 The Author(s). Published by Elsevier GmbH.. All rights reserved.)
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1016/j.molmet.2021.101244" target="_blank" rel="noreferrer noopener">10.1016/j.molmet.2021.101244</a>
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Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
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journalArticle
2021
Bawa FC
BILE acids
Department of Integrative Medical Sciences
Hu S
journalArticle
lipid absorption
Lipogenesis
May 2021 List
miR-34a
Molecular metabolism
NAFLD
NEOMED College of Medicine
NEOMED Postdoc Publications
NEOMED Student Publications
Pan X
Wang DQ
Wang HH
Xu Y
Yin L
Zhang Y
Zhu Y
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Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
URL Address
<table width="91" style="border-collapse:collapse;width:68pt;"><colgroup><col width="91" style="width:68pt;" /></colgroup><tbody><tr style="height:15pt;"><td width="91" height="20" class="xl18" style="width:68pt;height:15pt;"><a href="http://doi.org/10.1016/j.molmet.2021.101244">http://doi.org/10.1016/j.molmet.2021.101244</a></td>
</tr></tbody></table>
NEOMED College
NEOMED College of Medicine
NEOMED Department
Department of Integrative Medical Sciences
Update Year & Number
Jan to Aug list 2021
Dublin Core
The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/.
Title
A name given to the resource
Hepatocyte miR-34a is a key regulator in the development and progression of non-alcoholic fatty liver disease.
Creator
An entity primarily responsible for making the resource
Xu Y; Zhu Y; Hu S; Pan X; Bawa FC; Wang HH; Wang DQ; Yin L; Zhang Y
Publisher
An entity responsible for making the resource available
Molecular Metabolism
Date
A point or period of time associated with an event in the lifecycle of the resource
2021
2021-05-15
Description
An account of the resource
Hepatic miR-34a expression is elevated in diet-induced or genetically obese mice and patients with non-alcoholic steatohepatitis (NASH), yet hepatocyte miR-34a's role in the progression of non-alcoholic fatty liver disease (NAFLD) from non-alcoholic fatty liver (NAFL) to NASH remains to be elucidated.
Subject
The topic of the resource
Mice overexpressing or deficient in hepatocyte miR-34a and control mice were fed a diet enriched in fats, cholesterol, and fructose (HFCF) to induce NASH. C57BL/6 mice with NASH were treated with an miR-34a inhibitor or a scramble control oligo. The effect of miR-34a on the development, progression, and reversal of NAFLD was determined.
Identifier
An unambiguous reference to the resource within a given context
<table width="91" style="border-collapse:collapse;width:68pt;"><colgroup><col width="91" style="width:68pt;" /></colgroup><tbody><tr style="height:15pt;"><td width="91" height="20" class="xl18" style="width:68pt;height:15pt;"><a href="http://doi.org/10.1016/j.molmet.2021.101244">http://doi.org/10.1016/j.molmet.2021.101244</a></td>
</tr></tbody></table>
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Elsevier has partnered with Copyright Clearance Center's RightsLink service to offer a variety of options for reusing this content.
Format
The file format, physical medium, or dimensions of the resource
Journal Article
2021
bile acid
lipid absorption
Lipogenesis
miR-34a
NAFLD
-
Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
URL Address
<a href="http://doi.org/10.1016/j.ymthe.2019.09.008" target="_blank" rel="noreferrer noopener">http://doi.org/10.1016/j.ymthe.2019.09.008</a>
Rights
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
ISSN
1525-0016
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<a href="http://ezproxy.neomed.idm.oclc.org/login?url=http://doi.org/10.1016/j.ymthe.2019.09.008" target="_blank" rel="noreferrer noopener">NEOMED Full-text Holding (if available) - Proxy DOI: 10.1016/j.ymthe.2019.09.008</a>
<p>Users with a NEOMED Library login can search for full-text journal articles at the following url: <a href="https://libraryguides.neomed.edu/home">https://libraryguides.neomed.edu/home</a></p>
Dublin Core
The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/.
Title
A name given to the resource
Macrophage miR-34a Is a Key Regulator of Cholesterol Efflux and Atherosclerosis
Publisher
An entity responsible for making the resource available
Molecular Therapy
Date
A point or period of time associated with an event in the lifecycle of the resource
2019
2019-01-01
Subject
The topic of the resource
atherosclerosis; inflammation; cholesterol efflux; ABCA1; ABCG1; LXR; miR-34a
Creator
An entity primarily responsible for making the resource
Xu Yanyong; Xu Yang; Zhu Yingdong; Sun Huihui; Juguilon Cody; Li Feng; Fan Daping; Yin Liya; Zhang Yanqiao
Description
An account of the resource
Macrophages play a crucial role in the pathogenesis of atherosclerosis, but the molecular mechanisms remain poorly understood. Here we show that microRNA-34a (miR-34a) is a key regulator of macrophage cholesterol efflux and reverse cholesterol transport by modulating ATP-binding cassette transporters ATP-binding cassette subfamily A member 1 (ABCA1) and ATP-binding cassette subfamily G member 1 (ABCG1). miR-34a also regulates M1 and M2 macrophage polarization via liver X receptor α. Furthermore, global loss of miR-34a reduces intestinal cholesterol or fat absorption by inhibiting cytochrome P450 enzymes CYP7A1 and sterol 12α-hydroxylase (CYP8B1). Consistent with these findings, macrophage-selective or global ablation of miR-34a markedly inhibits the development of atherosclerosis. Finally, therapeutic inhibition of miR-34a promotes atherosclerosis regression and reverses diet-induced metabolic disorders. Our studies outline a central role of miR-34a in regulating macrophage cholesterol efflux, inflammation, and atherosclerosis, suggesting that miR-34a is a promising target for treatment of cardiometabolic diseases.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1016/j.ymthe.2019.09.008" target="_blank" rel="noreferrer noopener">10.1016/j.ymthe.2019.09.008</a>
Format
The file format, physical medium, or dimensions of the resource
Journal Article
2019
ABCA1
ABCG1
Atherosclerosis
cholesterol efflux
Department of Integrative Medical Sciences
Fan Daping
Inflammation
Journal Article
Juguilon Cody
Li Feng
LXR
miR-34a
Molecular Therapy
NEOMED College of Graduate Studies Student
NEOMED College of Medicine
November 2019 Update
Sun Huihui
Xu Yang
Xu Yanyong
Yin Liya
Zhang Yanqiao
Zhu Yingdong