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http://hdl.handle.net/2445/208403
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DC Field | Value | Language |
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dc.contributor.author | Yáñez Bisbe, Laia | - |
dc.contributor.author | Moya, Mar | - |
dc.contributor.author | Rodríguez Sinovas, Antonio | - |
dc.contributor.author | Ruiz Meana, Marisol | - |
dc.contributor.author | Inserte, Javier | - |
dc.contributor.author | Tajes, Marta | - |
dc.contributor.author | Batlle, Montserrat | - |
dc.contributor.author | Guasch, Eduard | - |
dc.contributor.author | Mas Stachurska, Aleksandra | - |
dc.contributor.author | Miró, Elisabet | - |
dc.contributor.author | Rivas, Nuria | - |
dc.contributor.author | Ferreira González, Ignacio | - |
dc.contributor.author | Garcia Elias, Anna | - |
dc.contributor.author | Benito, Begoña | - |
dc.date.accessioned | 2024-03-05T12:31:11Z | - |
dc.date.available | 2024-03-05T12:31:11Z | - |
dc.date.issued | 2024-01-26 | - |
dc.identifier.issn | 1422-0067 | - |
dc.identifier.uri | http://hdl.handle.net/2445/208403 | - |
dc.description.abstract | TRPV4 channels, which respond to mechanical activation by permeating Ca2+ into the cell, may play a pivotal role in cardiac remodeling during cardiac overload. Our study aimed to investigate TRPV4 involvement in pathological and physiological remodeling through Ca2+-dependent signaling. TRPV4 expression was assessed in heart failure (HF) models, induced by isoproterenol infusion or transverse aortic constriction, and in exercise-induced adaptive remodeling models. The impact of genetic TRPV4 inhibition on HF was studied by echocardiography, histology, gene and protein analysis, arrhythmia inducibility, Ca2+ dynamics, calcineurin (CN) activity, and NFAT nuclear translocation. TRPV4 expression exclusively increased in HF models, strongly correlating with fibrosis. Isoproterenol-administered transgenic TRPV4-/- mice did not exhibit HF features. Cardiac fibroblasts (CFb) from TRPV4+/+ animals, compared to TRPV4-/-, displayed significant TRPV4 overexpression, elevated Ca2+ influx, and enhanced CN/NFATc3 pathway activation. TRPC6 expression paralleled that of TRPV4 in all models, with no increase in TRPV4-/- mice. In cultured CFb, the activation of TRPV4 by GSK1016790A increased TRPC6 expression, which led to enhanced CN/NFATc3 activation through synergistic action of both channels. In conclusion, TRPV4 channels contribute to pathological remodeling by promoting fibrosis and inducing TRPC6 upregulation through the activation of Ca2+-dependent CN/NFATc3 signaling. These results pose TRPV4 as a primary mediator of the pathological response. | - |
dc.format.extent | 20 p. | - |
dc.format.mimetype | application/pdf | - |
dc.language.iso | eng | - |
dc.publisher | MDPI AG | - |
dc.relation.isformatof | Reproducció del document publicat a: https://doi.org/10.3390/ijms25031541 | - |
dc.relation.ispartof | International Journal of Molecular Sciences, 2024, vol. 25, num. 3, p. 1541 | - |
dc.relation.uri | https://doi.org/10.3390/ijms25031541 | - |
dc.rights | cc by (c) Yáñez Bisbe, Laia et al., 2024 | - |
dc.rights.uri | http://creativecommons.org/licenses/by/3.0/es/ | * |
dc.source | Articles publicats en revistes (Institut d'lnvestigació Biomèdica de Bellvitge (IDIBELL)) | - |
dc.subject.classification | Insuficiència cardíaca | - |
dc.subject.classification | Ratolins transgènics | - |
dc.subject.other | Heart Failure | - |
dc.subject.other | Mice, Transgenic | - |
dc.title | TRPV4 Channels Promote Pathological, but Not Physiological, Cardiac Remodeling through the Activation of Calcineurin/NFAT and TRPC6 | - |
dc.type | info:eu-repo/semantics/article | - |
dc.type | info:eu-repo/semantics/publishedVersion | - |
dc.date.updated | 2024-02-26T12:46:16Z | - |
dc.rights.accessRights | info:eu-repo/semantics/openAccess | - |
dc.identifier.pmid | 38338818 | - |
Appears in Collections: | Articles publicats en revistes (Institut d'lnvestigació Biomèdica de Bellvitge (IDIBELL)) |
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ijms-25-01541.pdf | 3.85 MB | Adobe PDF | View/Open |
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