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11/29/2024 2:50:18 PM | Browse: 168 | Download: 1179
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Received |
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2024-05-07 14:38 |
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Peer-Review Started |
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2024-05-07 14:38 |
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First Decision by Editorial Office Director |
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2024-08-25 02:14 |
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Return for Revision |
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2024-08-25 02:14 |
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Revised |
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2024-08-31 14:23 |
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Publication Fee Transferred |
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Second Decision by Editor |
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2024-09-18 02:41 |
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Second Decision by Editor-in-Chief |
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Final Decision by Editorial Office Director |
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2024-09-19 12:34 |
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Articles in Press |
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2024-09-19 12:34 |
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Edit the Manuscript by Language Editor |
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2024-10-28 22:25 |
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Typeset the Manuscript |
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2024-11-22 00:42 |
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Publish the Manuscript Online |
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2024-11-29 14:50 |
| ISSN |
1948-5182 (online) |
| Open Access |
This article is an open-access article that was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution NonCommercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: https://creativecommons.org/licenses/by-nc/4.0/ |
| Copyright |
© The Author(s) 2024. Published by Baishideng Publishing Group Inc. All rights reserved. |
| Article Reprints |
For details, please visit: http://www.wjgnet.com/bpg/gerinfo/247
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| Permissions |
For details, please visit: http://www.wjgnet.com/bpg/gerinfo/207
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| Publisher |
Baishideng Publishing Group Inc, 7041 Koll Center Parkway, Suite 160, Pleasanton, CA 94566, USA |
| Website |
http://www.wjgnet.com |
| Category |
Gastroenterology & Hepatology |
| Manuscript Type |
Basic Study |
| Article Title |
Lipophagy and epigenetic alterations are related to metabolic dysfunction-associated steatotic liver disease progression in an experimental model
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| Manuscript Source |
Unsolicited Manuscript |
| All Author List |
Felipe Schütz, Larisse Longo, Melina Belén Keingeski, Eduardo Filippi-Chiela, Carolina Uribe-Cruz and Mário Reis Álvares-da-Silva |
| ORCID |
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| Funding Agency and Grant Number |
| Funding Agency |
Grant Number |
| Financiamento e Incentivo à Pesquisa from Hospital de Clínicas de Porto Alegre (FIPE/HCPA) |
2022-0117 |
| National Council for Scientific and Technological Development |
CNPq |
| Coordination for the Improvement of Higher Education Personnel |
CAPES/PNPD |
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| Corresponding Author |
Mário Reis Álvares-da-Silva, MD, PhD, Professor, Experimental Laboratory of Hepatology and Gastroenterology, Hospital de Clínicas de Porto Alegre, Rua Ramiro Barcelos, n° 2350/Sala 2033, 2° Andar, Porto Alegre 90035-007, Rio Grande do Sul, Brazil. marioreis@live.com |
| Key Words |
Animal model; Epigenetic; Lipophagy; MicroRNAs; Metabolic dysfunction-associated steatotic liver disease; Metabolic dysfunction-associated steatohepatitis |
| Core Tip |
This nutritional model of metabolic dysfunction-associated steatohepatitis (MASH) is useful for evaluating pathophysiological mechanisms and therapeutic targets for metabolic dysfunction-associated steatotic liver disease (MASLD). Animals with MASH showed increased expression of miR-34a and miR-21, markers that contribute to the inflammatory process and fibrogenesis of the disease. Additionally, the lipophagy process was reduced due to increased perilipin gene expression and decreased Sirtuin-1. Lysosomal stress and autophagic activity increased in MASH, through increased expression of transcription factor-EB and decreased levels of p62/sequestosome-1. Alterations in the expression of these genes are related to the inflammatory process and fibrogenesis, processes that promote the progression of MASLD. |
| Publish Date |
2024-11-29 14:50 |
| Citation |
Schütz F, Longo L, Keingeski MB, Filippi-Chiela E, Uribe-Cruz C, Álvares-da-Silva MR. Lipophagy and epigenetic alterations are related to metabolic dysfunction-associated steatotic liver disease progression in an experimental model. World J Hepatol 2024; 16(12): 1468-1479 |
| URL |
https://www.wjgnet.com/1948-5182/full/v16/i12/1468.htm |
| DOI |
https://dx.doi.org/10.4254/wjh.v16.i12.1468 |
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