dc.contributor.author | Fondevila, Marcos F | |
dc.contributor.author | Novoa, Eva | |
dc.contributor.author | Gonzalez-Rellan, Maria J | |
dc.contributor.author | Fernandez, Uxia | |
dc.contributor.author | Heras, Violeta | |
dc.contributor.author | Porteiro, Begoña | |
dc.contributor.author | Parracho, Tamara | |
dc.contributor.author | Dorta, Valentina | |
dc.contributor.author | Riobello, Cristina | |
dc.contributor.author | da Silva Lima, Natalia | |
dc.contributor.author | Seoane, Samuel | |
dc.contributor.author | Garcia-Vence, Maria | |
dc.contributor.author | Chantada-Vazquez, Maria P | |
dc.contributor.author | Bravo, Susana B | |
dc.contributor.author | Senra, Ana | |
dc.contributor.author | Leiva, Magdalena | |
dc.contributor.author | Marcos, Miguel | |
dc.contributor.author | Sabio, Guadalupe | |
dc.contributor.author | Perez-Fernandez, Roman | |
dc.contributor.author | Dieguez, Carlos | |
dc.contributor.author | Prevot, Vincent | |
dc.contributor.author | Schwaninger, Markus | |
dc.contributor.author | Woodhoo, Ashwin | |
dc.contributor.author | Martinez-Chantar, Maria L | |
dc.contributor.author | Schwabe, Robert | |
dc.contributor.author | Cubero, Francisco J | |
dc.contributor.author | Varela-Rey, Marta | |
dc.contributor.author | Crespo, Javier | |
dc.contributor.author | Iruzubieta, Paula | |
dc.contributor.author | Nogueiras, Ruben | |
dc.date.accessioned | 2024-07-03T14:55:31Z | |
dc.date.available | 2024-07-03T14:55:31Z | |
dc.date.issued | 2024-02-20 | |
dc.identifier.citation | Cell Rep Med. 2024 Feb 20;5(2):101401. | es_ES |
dc.identifier.uri | http://hdl.handle.net/20.500.12105/20037 | |
dc.description.abstract | The p63 protein has pleiotropic functions and, in the liver, participates in the progression of nonalcoholic fatty liver disease (NAFLD). However, its functions in hepatic stellate cells (HSCs) have not yet been explored. TAp63 is induced in HSCs from animal models and patients with liver fibrosis and its levels positively correlate with NAFLD activity score and fibrosis stage. In mice, genetic depletion of TAp63 in HSCs reduces the diet-induced liver fibrosis. In vitro silencing of p63 blunts TGF-β1-induced HSCs activation by reducing mitochondrial respiration and glycolysis, as well as decreasing acetyl CoA carboxylase 1 (ACC1). Ectopic expression of TAp63 induces the activation of HSCs and increases the expression and activity of ACC1 by promoting the transcriptional activity of HER2. Genetic inhibition of both HER2 and ACC1 blunt TAp63-induced activation of HSCs. Thus, TAp63 induces HSC activation by stimulating the HER2-ACC1 axis and participates in the development of liver fibrosis. | es_ES |
dc.description.sponsorship | This work has been supported by grants from FEDER/Ministerio de Ciencia,
Innovacio´ n y Universidades-Agencia Estatal de Investigacio´ n (M.L.M.-C.:
RTC2019-007125-1and SAF2017-87301-R; C.D.: PID2020-116628GB-100;
R.N.: PID2021-126096NB-I00 and RED2018-102379-T; M.V.-R.: PID2020-
119486RB-100; A.W.: PID2021-127169OB-I00), Xunta de Galicia (R.N.:
2021-CP085 and 2020-PG015), Fundacio´ n BBVA (R.N., M.L.M.-C., and
G.S.), Proyectos Investigacio´ n en Salud (M.L.M.-C.: DTS20/00138), Fundacion Araucaria (R.N.), and European Foundation for the Study of Diabetes
(R.N.). This research also received funding from the European Community’s
H2020 Framework Programme (ERC Synergy Grant-2019-WATCH- 810331,
to R.N., V.P., and M.S. and ERC Consolidator grant no. 865157 to A.W.;
MSCA Doctoral Networks 2021 no. 101073094 to A.W. and M.V.-R.). Centro
de Investigacio´ n Biome´ dica en Red (CIBER) de Fisiopatologı´a de la Obesidad
y Nutricio´ n (CIBERobn), Centro de Investigacio´ n Biome´ dica en Red (CIBER) de
Enfermedades Hepa´ticas y Digestivas (CIBERehd). CIBERobn, and CIBERehd
are initiatives of the Instituto de Salud Carlos III (ISCIII) of Spain, which is supported by FEDER funds. We thank MINECO for the Severo Ochoa Excellence
Accreditation to CIC bioGUNE (SEV-2016-0644). | es_ES |
dc.language.iso | eng | es_ES |
dc.publisher | Elsevier | es_ES |
dc.type.hasVersion | VoR | es_ES |
dc.rights.uri | http://creativecommons.org/licenses/by-nc-nd/4.0/ | * |
dc.subject.mesh | Hepatic Stellate Cells | es_ES |
dc.subject.mesh | Non-alcoholic Fatty Liver Disease | es_ES |
dc.subject.mesh | Humans | es_ES |
dc.subject.mesh | Mice | es_ES |
dc.subject.mesh | Animals | es_ES |
dc.subject.mesh | Activation, Metabolic | es_ES |
dc.subject.mesh | Liver Cirrhosis | es_ES |
dc.subject.mesh | Fibrosis | es_ES |
dc.subject.mesh | Acetyl-CoA Carboxylase | es_ES |
dc.title | p63 controls metabolic activation of hepatic stellate cells and fibrosis via an HER2-ACC1 pathway. | es_ES |
dc.type | journal article | es_ES |
dc.rights.license | Attribution-NonCommercial-NoDerivatives 4.0 Internacional | * |
dc.identifier.pubmedID | 38340725 | es_ES |
dc.format.volume | 5 | es_ES |
dc.format.number | 2 | es_ES |
dc.format.page | 101401 | es_ES |
dc.identifier.doi | 10.1016/j.xcrm.2024.101401 | es_ES |
dc.contributor.funder | Unión Europea. Fondo Europeo de Desarrollo Regional (FEDER/ERDF) | es_ES |
dc.contributor.funder | Ministerio de Ciencia, Innovación y Universidades (España) | es_ES |
dc.contributor.funder | Agencia Estatal de Investigación (España) | es_ES |
dc.contributor.funder | Xunta de Galicia (España) | es_ES |
dc.contributor.funder | Fundación BBVA | es_ES |
dc.contributor.funder | European Foundation for the Study of Diabetes | es_ES |
dc.contributor.funder | Unión Europea. Comisión Europea. H2020 | es_ES |
dc.contributor.funder | Centro de Investigación Biomédica en Red - CIBEROBN (Fisiopatología de la Obesidad y Nutrición) | es_ES |
dc.contributor.funder | Instituto de Salud Carlos III | es_ES |
dc.contributor.funder | Ministerio de Ciencia e Innovación. Centro de Excelencia Severo Ochoa (España) | es_ES |
dc.description.peerreviewed | Sí | es_ES |
dc.identifier.e-issn | 2666-3791 | es_ES |
dc.relation.publisherversion | 10.1016/j.xcrm.2024.101401 | es_ES |
dc.identifier.journal | Cell reports. Medicine | es_ES |
dc.repisalud.orgCNIC | CNIC::Grupos de investigación::Papel de las quinasas activadas por el estrés en el desarrollo de enfermedades cardiovasculares, diabetes y cáncer | es_ES |
dc.repisalud.institucion | CNIC | es_ES |
dc.rights.accessRights | open access | es_ES |
dc.relation.projectFECYT | info:eu-repo/grantAgreement/ES/RTC2019-007125-1 | es_ES |
dc.relation.projectFECYT | info:eu-repo/grantAgreement/ES/SAF2017-87301-R | es_ES |
dc.relation.projectFECYT | info:eu-repo/grantAgreement/ES/PID2020-116628GB-100 | es_ES |
dc.relation.projectFECYT | info:eu-repo/grantAgreement/ES/PID2021-126096NB-I00 | es_ES |
dc.relation.projectFECYT | info:eu-repo/grantAgreement/ES/RED2018-102379-T | es_ES |
dc.relation.projectFECYT | info:eu-repo/grantAgreement/ES/PID2020-119486RB-100 | es_ES |
dc.relation.projectFECYT | info:eu-repo/grantAgreement/ES/PID2021-127169OB-I00 | es_ES |
dc.relation.projectFECYT | info:eu-repo/grantAgreement/ES/2021-CP085 | es_ES |
dc.relation.projectFECYT | info:eu-repo/grantAgreement/ES/2020-PG015 | es_ES |
dc.relation.projectFECYT | info:eu-repo/grantAgreement/ES/SEV-2016-0644 | es_ES |