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

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Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License (CC-BY-NC-ND 4.0)
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Título
Specialized proresolving mediators protect against experimental autoimmune myocarditis by modulating Ca2+ handling and NRF2 activation
Autor(es)
Data
2022-05-18
Cita bibliográfica
Val-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.
Resumo
[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.
Palabras chave
Calcium handling
Myocarditis
NRF2
Pro-resolving mediators
SERCA2A
 
Descrición
Preclinical research
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Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License (CC-BY-NC-ND 4.0)
ISSN
2452-302X