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Specialized Proresolving Mediators Protect Against Experimental Autoimmune Myocarditis by Modulating Ca2+ Handling and NRF2 Activation

2022; Elsevier BV; Volume: 7; Issue: 6 Linguagem: Inglês

10.1016/j.jacbts.2022.01.009

2452-302X

Almudena Val‐Blasco, Patricia Prieto, Rafael I. Jaén, Marta Gil-Fernández, Marta Pajares, Nieves Doménech, Verónica Terrón, María Tamayo, Inmaculada Jorge, Jesús Vázquez, Andrea Bueno-Sen, María Teresa Vallejo‐Cremades, Jorge Pombo-Otero, Sergio Sánchez‐García, Gema Ruiz‐Hurtado, Ana M. Gómez, Carlos Zaragoza, María G. Crespo‐Leiro, Eduardo López‐Collazo, Antonio Cuadrado, Carmen Delgado, Lisardo Boscá, María Fernández‐Velasco,

Galectins and Cancer Biology

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.