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oai:repisalud.isciii.es:20.500.12105/157532024-09-27T09:57:51Zcom_20.500.12105_19604com_20.500.12105_2051col_20.500.12105_19605

00925njm 22002777a 4500 dc Val-Blasco, Almudena author Prieto, Patricia author Jaén, Rafael Iñigo author Gil-Fernández, Marta author Pajares, Marta author Domenech, Nieves author Terrón, Verónica author Tamayo, María author Jorge, Inmaculada author Vazquez, Jesus author Bueno-Sen, Andrea author Vallejo-Cremades, María Teresa author Pombo-Otero, Jorge author Sanchez-García, Sergio author Ruiz-Hurtado, Gema author Gómez, Ana María author Zaragoza, Carlos author Crespo-Leiro, María Generosa author López-Collazo, Eduardo author Cuadrado, Antonio author Delgado, Carmen author Boscá, Lisardo author Fernández-Velasco, María author 2022-06 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. JACC Basic Transl Sci. 2022 May 18; 7(6):544-560 10.1016/j.jacbts.2022.01.009 2452-302X JACC. Basic to translational science 35818504 http://hdl.handle.net/20.500.12105/15753 Specialized Proresolving Mediators Protect Against Experimental Autoimmune Myocarditis by Modulating Ca2+ Handling and NRF2 Activation.