dc.creator | Rojas, Angela | es |
dc.creator | Garcia-Lozano, Maria Rosario | es |
dc.creator | Gil-Gomez, Antonio | es |
dc.creator | Romero Gómez, Manuel | es |
dc.creator | Ampuero Herrojo, Javier | es |
dc.date.accessioned | 2022-11-17T14:28:34Z | |
dc.date.available | 2022-11-17T14:28:34Z | |
dc.date.issued | 2022 | |
dc.identifier.citation | Rojas, A., Garcia-Lozano, M.R., Gil-Gomez, A., Romero Gómez, M. y Ampuero Herrojo, J. (2022). Glutaminolysis-ammonia-urea Cycle Axis, Non-alcoholic Fatty Liver Disease Progression and Development of Novel Therapies. Journal of Clinical and Translational Hepatology, 10 (2), 356-362. https://doi.org/10.14218/JCTH.2021.00247. | |
dc.identifier.issn | 2225-0719 | es |
dc.identifier.issn | 2310-8819 | es |
dc.identifier.uri | https://hdl.handle.net/11441/139558 | |
dc.description.abstract | 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. | es |
dc.format | application/pdf | es |
dc.format.extent | 7 p. | es |
dc.language.iso | eng | es |
dc.publisher | XHP Publishing | es |
dc.relation.ispartof | Journal of Clinical and Translational Hepatology, 10 (2), 356-362. | |
dc.rights | Atribución-NoComercial 4.0 Internacional | * |
dc.rights.uri | http://creativecommons.org/licenses/by-nc/4.0/ | * |
dc.subject | Non-alcoholic fatty liver disease (NAFLD) | es |
dc.subject | Cirrhosis | es |
dc.subject | Fibrosis | es |
dc.subject | Glutaminolysis | es |
dc.subject | Ammonia | es |
dc.subject | Urea | es |
dc.title | Glutaminolysis-ammonia-urea Cycle Axis, Non-alcoholic Fatty Liver Disease Progression and Development of Novel Therapies | es |
dc.type | info:eu-repo/semantics/article | es |
dcterms.identifier | https://ror.org/03yxnpp24 | |
dc.type.version | info:eu-repo/semantics/publishedVersion | es |
dc.rights.accessRights | info:eu-repo/semantics/openAccess | es |
dc.contributor.affiliation | Universidad de Sevilla. Departamento de Medicina | es |
dc.relation.publisherversion | https://www.xiahepublishing.com/2310-8819/JCTH-2021-00247 | es |
dc.identifier.doi | 10.14218/JCTH.2021.00247 | es |
dc.journaltitle | Journal of Clinical and Translational Hepatology | es |
dc.publication.volumen | 10 | es |
dc.publication.issue | 2 | es |
dc.publication.initialPage | 356 | es |
dc.publication.endPage | 362 | es |