Please use this identifier to cite or link to this item:http://hdl.handle.net/20.500.12105/15753
Title
Specialized Proresolving Mediators Protect Against Experimental Autoimmune Myocarditis by Modulating Ca2+ Handling and NRF2 Activation.
Author(s)
Val-Blasco, Almudena | Prieto, Patricia | Jaén, Rafael Iñigo | Gil-Fernández, Marta | Pajares, Marta | Domenech, Nieves | Terrón, Verónica | Tamayo, María | Jorge, Inmaculada CNIC | Vazquez, Jesus CNIC | Bueno-Sen, Andrea | Vallejo-Cremades, María Teresa | Pombo-Otero, Jorge | Sanchez-García, Sergio | Ruiz-Hurtado, Gema | Gómez, Ana María | Zaragoza, Carlos CNIC | Crespo-Leiro, María Generosa | López-Collazo, Eduardo | Cuadrado, Antonio | Delgado, Carmen | Boscá, Lisardo | Fernández-Velasco, María
Date issued
2022-06
Citation
JACC Basic Transl Sci. 2022 May 18; 7(6):544-560
Language
Inglés
Document type
journal article
Abstract
Specialized proresolving mediators and, in particular, 5(S), (6)R, 7-trihydroxyheptanoic acid methyl ester (BML-111) emerge as new therapeutic tools to prevent cardiac dysfunction and deleterious cardiac damage associated with myocarditis progression. The cardioprotective role of BML-111 is mainly caused by the prevention of increased oxidative stress and nuclear factor erythroid-derived 2-like 2 (NRF2) down-regulation induced by myocarditis. At the molecular level, BML-111 activates NRF2 signaling, which prevents sarcoplasmic reticulum-adenosine triphosphatase 2A down-regulation and Ca2+ mishandling, and attenuates the cardiac dysfunction and tissue damage induced by myocarditis.
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