Por favor, use este identificador para citar o enlazar este ítem:
https://repositorio.uca.edu.ar/handle/123456789/9853
Campo DC | Valor | Lengua/Idioma |
---|---|---|
dc.contributor.author | Saliba, Youakim | es |
dc.contributor.author | Jebara, Victor | es |
dc.contributor.author | Hajal, Joelle | es |
dc.contributor.author | Maroun, Richard | es |
dc.contributor.author | Chacar, Stéphanie | es |
dc.contributor.author | Smayra, Viviane | es |
dc.contributor.author | Abramowitz, Joel | es |
dc.contributor.author | Birnbaumer, Lutz | es |
dc.contributor.author | Farès, Nassim | es |
dc.date.accessioned | 2020-05-04T20:38:07Z | - |
dc.date.available | 2020-05-04T20:38:07Z | - |
dc.date.issued | 2019 | - |
dc.identifier.citation | Saliba, Y. et al. Transient Receptor Potential Canonical 3 and nuclear factor of activated T cells C3 signaling pathway critically regulates myocardial fibrosis [en línea]. Antioxidants & Redox Signaling. 2019, 30(16). doi:10.1089/ars.2018.7545 Disponible en: https://repositorio.uca.edu.ar/handle/123456789/9853 | es |
dc.identifier.issn | 1523-0864 (impreso) | - |
dc.identifier.issn | 1557-7716 (online) | - |
dc.identifier.uri | https://repositorio.uca.edu.ar/handle/123456789/9853 | - |
dc.description.abstract | Abstract: Aims: Cardiac fibroblasts (CFs) are emerging as major contributors to myocardial fibrosis (MF), a final common pathway of many etiologies of heart disease. Here, we studied the functional relevance of transient receptor potential canonical 3 (TRPC3) channels and nuclear factor of activated T cells c3 (NFATc3) signaling in rodent and human ventricular CFs, and whether their modulation would limit MF. Results: A positive feedback loop between TRPC3 and NFATc3 drove a rat ventricular CF fibrotic phenotype. In these cells, polyphenols (extract of grape pomace polyphenol [P.E.]) decreased basal and angiotensin II-mediated Ca2+ entries through a direct modulation of TRPC3 channels and subsequently NFATc3 signaling, abrogating myofibroblast differentiation, fibrosis and inflammation, as well as an oxidative stress-associated phenotype. N(ω)-nitro-l-arginine methyl ester (l-NAME) hypertensive rats developed coronary perivascular, sub-epicardial, and interstitial fibrosis with induction of embryonic epicardial progenitor transcription factors in activated CFs. P.E. treatment reduced ventricular CF activation by modulating the TRPC3-NFATc3 pathway, and it ameliorated echocardiographic parameters, cardiac stress markers, and MF in l-NAME hypertensive rats independently of blood pressure regulation. Further, genetic deletion (TRPC3−/−) and pharmacological channel blockade with N-[4-[3,5-Bis(trifluoromethyl)-1H-pyrazol-1-yl]phenyl]-4-methyl-benzenesulfonamide (Pyr10) blunted ventricular CF activation and MF in l-NAME hypertensive mice. Finally, TRPC3 was present in human ventricular CFs and upregulated in MF, whereas pharmacological modulation of TRPC3-NFATc3 decreased proliferation and collagen secretion. Innovation and Conclusion: We demonstrate that TRPC3-NFATc3 signaling is modulated by P.E. and critically regulates ventricular CF phenotype and MF. These findings strongly argue for P.E., through TRPC3 targeting, as potential and interesting therapeutics for MF management. | es |
dc.format | application/pdf | es |
dc.language.iso | eng | es |
dc.publisher | Mary Ann Liebert | es |
dc.rights | Acceso abierto | * |
dc.rights.uri | http://creativecommons.org/licenses/by-nc-sa/4.0/ | * |
dc.source | Antioxidants & Redox Signaling. 2019, 30(16) | es |
dc.subject | TRPC3 | es |
dc.subject | CALCIO | es |
dc.subject | FIBROSIS | es |
dc.subject | POLIFENOLES | es |
dc.subject | CARDIOPATIAS | es |
dc.subject | TRATAMIENTO MEDICO | es |
dc.title | Transient Receptor Potential Canonical 3 and nuclear factor of activated T cells C3 signaling pathway critically regulates myocardial fibrosis | es |
dc.type | Artículo | es |
dc.identifier.doi | 10.1089/ars.2018.7545 | - |
dc.identifier.pmid | 30318928 | - |
uca.disciplina | MEDICINA | es |
uca.issnrd | 1 | es |
uca.affiliation | Fil: Saliba, Youakim. Université Saint Joseph. Faculté de Médecine. Pôle Technologie Santé. Laboratoire de Recherche en Physiologie et Physiopathologie; Líbano | es |
uca.affiliation | Fil: Jebara, Victor. Université Saint Joseph. Faculté de Médecine; Líbano | es |
uca.affiliation | Fil: Hajal, Joelle. Université Saint Joseph. Faculté de Médecine. Pôle Technologie Santé. Laboratoire de Recherche en Physiologie et Physiopathologie; Líbano | es |
uca.affiliation | Fil: Maroun, Richard. Université Saint‐Joseph. Faculté des Sciences. Unité de Recherche Technologie et Valorisation Alimentaire. Centre d'Analyses et de Recherche; Líbano | es |
uca.affiliation | Fil: Chacar, Stéphanie. Université Saint Joseph. Faculté de Médecine. Pôle Technologie Santé. Laboratoire de Recherche en Physiologie et Physiopathologie; Líbano | es |
uca.affiliation | Fil: Chacar, Stéphanie. Université Saint‐Joseph. Faculté des Sciences. Unité de Recherche Technologie et Valorisation Alimentaire. Centre d'Analyses et de Recherche; Líbano | es |
uca.affiliation | Fil: Smayra, Viviane. Université Saint Joseph. Faculté de Médecine; Líbano | es |
uca.affiliation | Fil: Abramowitz, Joel. National Institute of Environmental Health Sciences. Neurobiology Laboratory; Estados Unidos | es |
uca.affiliation | Fil: Birnbaumer, Lutz. National Institute of Environmental Health Sciences. Neurobiology Laboratory; Estados Unidos | es |
uca.affiliation | Fil: Birnbaumer, Lutz. Pontificia Universidad Católica Argentina. Facultad de Ciencais Médicas. Instituto de Investigaciones Biomédicas; Argentina | es |
uca.affiliation | Fil: Farès, Nassim. Université Saint Joseph. Faculté de Médecine. Pôle Technologie Santé. Laboratoire de Recherche en Physiologie et Physiopathologie; Líbano | es |
uca.version | acceptedVersion | es |
item.grantfulltext | open | - |
item.languageiso639-1 | en | - |
item.fulltext | With Fulltext | - |
crisitem.author.dept | Instituto de Investigaciones Biomédicas - BIOMED | - |
crisitem.author.dept | Laboratorio de Función y Farmacología de Canales Iónicos | - |
crisitem.author.dept | Consejo Nacional de Investigaciones Científicas y Técnicas | - |
crisitem.author.dept | Facultad de Ciencias Médicas | - |
crisitem.author.orcid | 0000-0002-0775-8661 | - |
crisitem.author.parentorg | Facultad de Ciencias Médicas | - |
crisitem.author.parentorg | Instituto de Investigaciones Biomédicas - BIOMED | - |
crisitem.author.parentorg | Pontificia Universidad Católica Argentina | - |
Aparece en las colecciones: | Artículos |
Ficheros en este ítem:
Fichero | Descripción | Tamaño | Formato | |
---|---|---|---|---|
transient-receptor-potential-birnbaumer.pdf | 5,81 MB | Adobe PDF | Visualizar/Abrir |
Visualizaciones de página(s)
80
comprobado en 30-abr-2024
Descarga(s)
136
comprobado en 30-abr-2024
Google ScholarTM
Consultar
Altmetric
Este ítem está sujeto a una licencia Creative Commons Licencia Creative Commons