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2 results on '"Bueno-Sen, A."'

1. Specialized proresolving mediators protect against experimental autoimmune myocarditis by modulating Ca2+ handling and NRF2 activation

Author

Ministerio de Ciencia, Innovación y Universidades (España), Agencia Estatal de Investigación (España), Instituto de Salud Carlos III, Sociedad Española de Cardiología, Fundación la Caixa, Val-Blasco, Almudena, Prieto, Patricia, Iñigo Jaén, Rafael, Gil-Fernández, Marta, Pajares, Marta, Domenech, N., Terrón, Verónica, Tamayo, María, Jorge, Inmaculada, Vázquez, Jesús, Bueno-Sen, A., Vallejo-Cremades, Maria T., Pombo-Otero, Jorge, Sánchez-García, Sergio, Ruiz-Hurtado, Gema, Gómez, Ana María, Zaragoza, Carlos, Crespo-Leiro, M. G., López-Collazo, Eduardo, Cuadrado, Antonio, Delgado, Carmen, Boscá, Lisardo, Fernández-Velasco, María, Ministerio de Ciencia, Innovación y Universidades (España), Agencia Estatal de Investigación (España), Instituto de Salud Carlos III, Sociedad Española de Cardiología, Fundación la Caixa, Val-Blasco, Almudena, Prieto, Patricia, Iñigo Jaén, Rafael, Gil-Fernández, Marta, Pajares, Marta, Domenech, N., Terrón, Verónica, Tamayo, María, Jorge, Inmaculada, Vázquez, Jesús, Bueno-Sen, A., Vallejo-Cremades, Maria T., Pombo-Otero, Jorge, Sánchez-García, Sergio, Ruiz-Hurtado, Gema, Gómez, Ana María, Zaragoza, Carlos, Crespo-Leiro, M. G., López-Collazo, Eduardo, Cuadrado, Antonio, Delgado, Carmen, Boscá, Lisardo, and Fernández-Velasco, María

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.

Published
2022

2. Specialized proresolving mediators protect against experimental autoimmune myocarditis by modulating Ca2+ handling and NRF2 activation

Author

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

Abstract

[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.

Published
2022

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