Val-Blasco, AlmudenaPrieto Chinchilla, PatriciaÍñigo Jaén, RafaelGil-Fernández, MartaPajares, MartaDoménech, NievesTerrón, VerónicaTamayo, MaríaJorge, InmaculadaVázquez, JesúsBueno-Sen, AndreaVallejo-Cremades, María TeresaPombo-Otero, JorgeSánchez-García, SergioRuiz-Hurtado, GemaGómez, Ana MaríaZaragoza, CarlosCrespo-Leiro, María GenerosaLópez-Collado, EduardoCuadrado, AntonioDelgado, CarmenBoscá, LisardoFernández-Velasco, María2022-10-032022-10-032022-05-18Val-Blasco A, Prieto P, Jaén RI, Gil-Fernández M, Pajares M, Domenech N, Terrón V, Tamayo M, Jorge I, Vázquez J, Bueno-Sen A, Vallejo-Cremades MT, Pombo-Otero J, Sanchez-García S, Ruiz-Hurtado G, Gómez AM, Zaragoza C, Crespo-Leiro MG, López-Collazo E, Cuadrado A, Delgado C, Boscá L, Fernández-Velasco M. Specialized proresolving mediators protect against experimental autoimmune myocarditis by modulating Ca2+ handling and NRF2 activation. JACC Basic Transl Sci. 2022 May 18;7(6):544-560.2452-302Xhttp://hdl.handle.net/2183/31752Preclinical research[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.engCreative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License (CC-BY-NC-ND 4.0)http://creativecommons.org/licenses/by-nc-nd/4.0/Calcium handlingMyocarditisNRF2Pro-resolving mediatorsSERCA2Ajournal articleopen access