Glutaminolysis-ammonia-urea Cycle Axis, Non-alcoholic Fatty Liver Disease Progression and Development of Novel Therapies

The prevalence of non-alcoholic fatty liver disease (NAFLD) is increasing worldwide, reflecting the current epidemics of obesity, insulin resistance, type 2 diabetes mellitus, and metabolic syndrome. NAFLD is characterized by the accu mulation of fat in the liver, and is known to be a cause of cir r...

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Autores: Rojas, Ángela, Garcia-Lozano, Maria Rosario, Gil Gómez, Antonio, Romero Gómez, Manuel, Ampuero Herrojo, Javier
Tipo de recurso: artículo
Estado:Versión publicada
Fecha de publicación:2022
País:España
Institución:Universidad de Sevilla (US)
Repositorio:idUS. Depósito de Investigación de la Universidad de Sevilla
OAI Identifier:oai:idus.us.es:11441/139558
Acceso en línea:https://hdl.handle.net/11441/139558
https://doi.org/10.14218/JCTH.2021.00247
Access Level:acceso abierto
Palabra clave:Non-alcoholic fatty liver disease (NAFLD)
Cirrhosis
Fibrosis
Glutaminolysis
Ammonia
Urea
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spelling Glutaminolysis-ammonia-urea Cycle Axis, Non-alcoholic Fatty Liver Disease Progression and Development of Novel TherapiesRojas, ÁngelaGarcia-Lozano, Maria RosarioGil Gómez, AntonioRomero Gómez, ManuelAmpuero Herrojo, JavierNon-alcoholic fatty liver disease (NAFLD)CirrhosisFibrosisGlutaminolysisAmmoniaUreaThe prevalence of non-alcoholic fatty liver disease (NAFLD) is increasing worldwide, reflecting the current epidemics of obesity, insulin resistance, type 2 diabetes mellitus, and metabolic syndrome. NAFLD is characterized by the accu mulation of fat in the liver, and is known to be a cause of cir rhosis. Although many pathways have been proposed, the cause of NAFLD-linked fibrosis progression is still unclear, which posed challenges for the development of new thera pies to prevent NASH-related cirrhosis and hepatocellular carcinoma. Cirrhosis is associated with activation of hepatic stellate cells (HSC) and accumulation of excess extracellular matrix proteins, and inhibiting the activation of HSCs would be expected to slow the progression of NAFLD-cirrhosis. Multiple molecular signals and pathways such as oxidative stress and glutaminolysis have been reported to promote HSC activation. Both mechanisms are plausible antifibrotic targets in NASH, as the activation of HSCs the proliferation of myofibroblasts depend on those processes. This review summarizes the role of the glutaminolysis-ammonia-urea cycle axis in the context of NAFLD progression, and shows how the axis could be a novel therapeutic target.XHP PublishingMedicina2022info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionapplication/pdfapplication/pdfhttps://hdl.handle.net/11441/139558https://doi.org/10.14218/JCTH.2021.00247reponame:idUS. Depósito de Investigación de la Universidad de Sevillainstname:Universidad de Sevilla (US)InglésJournal of Clinical and Translational Hepatology, 10 (2), 356-362.https://www.xiahepublishing.com/2310-8819/JCTH-2021-00247info:eu-repo/semantics/openAccessoai:idus.us.es:11441/1395582026-06-17T12:51:07Z
dc.title.none.fl_str_mv Glutaminolysis-ammonia-urea Cycle Axis, Non-alcoholic Fatty Liver Disease Progression and Development of Novel Therapies
title Glutaminolysis-ammonia-urea Cycle Axis, Non-alcoholic Fatty Liver Disease Progression and Development of Novel Therapies
spellingShingle Glutaminolysis-ammonia-urea Cycle Axis, Non-alcoholic Fatty Liver Disease Progression and Development of Novel Therapies
Rojas, Ángela
Non-alcoholic fatty liver disease (NAFLD)
Cirrhosis
Fibrosis
Glutaminolysis
Ammonia
Urea
title_short Glutaminolysis-ammonia-urea Cycle Axis, Non-alcoholic Fatty Liver Disease Progression and Development of Novel Therapies
title_full Glutaminolysis-ammonia-urea Cycle Axis, Non-alcoholic Fatty Liver Disease Progression and Development of Novel Therapies
title_fullStr Glutaminolysis-ammonia-urea Cycle Axis, Non-alcoholic Fatty Liver Disease Progression and Development of Novel Therapies
title_full_unstemmed Glutaminolysis-ammonia-urea Cycle Axis, Non-alcoholic Fatty Liver Disease Progression and Development of Novel Therapies
title_sort Glutaminolysis-ammonia-urea Cycle Axis, Non-alcoholic Fatty Liver Disease Progression and Development of Novel Therapies
dc.creator.none.fl_str_mv Rojas, Ángela
Garcia-Lozano, Maria Rosario
Gil Gómez, Antonio
Romero Gómez, Manuel
Ampuero Herrojo, Javier
author Rojas, Ángela
author_facet Rojas, Ángela
Garcia-Lozano, Maria Rosario
Gil Gómez, Antonio
Romero Gómez, Manuel
Ampuero Herrojo, Javier
author_role author
author2 Garcia-Lozano, Maria Rosario
Gil Gómez, Antonio
Romero Gómez, Manuel
Ampuero Herrojo, Javier
author2_role author
author
author
author
dc.contributor.none.fl_str_mv Medicina
dc.subject.none.fl_str_mv Non-alcoholic fatty liver disease (NAFLD)
Cirrhosis
Fibrosis
Glutaminolysis
Ammonia
Urea
topic Non-alcoholic fatty liver disease (NAFLD)
Cirrhosis
Fibrosis
Glutaminolysis
Ammonia
Urea
description The prevalence of non-alcoholic fatty liver disease (NAFLD) is increasing worldwide, reflecting the current epidemics of obesity, insulin resistance, type 2 diabetes mellitus, and metabolic syndrome. NAFLD is characterized by the accu mulation of fat in the liver, and is known to be a cause of cir rhosis. Although many pathways have been proposed, the cause of NAFLD-linked fibrosis progression is still unclear, which posed challenges for the development of new thera pies to prevent NASH-related cirrhosis and hepatocellular carcinoma. Cirrhosis is associated with activation of hepatic stellate cells (HSC) and accumulation of excess extracellular matrix proteins, and inhibiting the activation of HSCs would be expected to slow the progression of NAFLD-cirrhosis. Multiple molecular signals and pathways such as oxidative stress and glutaminolysis have been reported to promote HSC activation. Both mechanisms are plausible antifibrotic targets in NASH, as the activation of HSCs the proliferation of myofibroblasts depend on those processes. This review summarizes the role of the glutaminolysis-ammonia-urea cycle axis in the context of NAFLD progression, and shows how the axis could be a novel therapeutic target.
publishDate 2022
dc.date.none.fl_str_mv 2022
dc.type.none.fl_str_mv info:eu-repo/semantics/article
info:eu-repo/semantics/publishedVersion
format article
status_str publishedVersion
dc.identifier.none.fl_str_mv https://hdl.handle.net/11441/139558
https://doi.org/10.14218/JCTH.2021.00247
url https://hdl.handle.net/11441/139558
https://doi.org/10.14218/JCTH.2021.00247
dc.language.none.fl_str_mv Inglés
language_invalid_str_mv Inglés
dc.relation.none.fl_str_mv Journal of Clinical and Translational Hepatology, 10 (2), 356-362.
https://www.xiahepublishing.com/2310-8819/JCTH-2021-00247
dc.rights.none.fl_str_mv info:eu-repo/semantics/openAccess
eu_rights_str_mv openAccess
dc.format.none.fl_str_mv application/pdf
application/pdf
dc.publisher.none.fl_str_mv XHP Publishing
publisher.none.fl_str_mv XHP Publishing
dc.source.none.fl_str_mv reponame:idUS. Depósito de Investigación de la Universidad de Sevilla
instname:Universidad de Sevilla (US)
instname_str Universidad de Sevilla (US)
reponame_str idUS. Depósito de Investigación de la Universidad de Sevilla
collection idUS. Depósito de Investigación de la Universidad de Sevilla
repository.name.fl_str_mv
repository.mail.fl_str_mv
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