Specialized proresolving mediators protect against experimental autoimmune myocarditis by modulating Ca2+ handling and NRF2 activation
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A non ser que se indique outra cousa, a licenza do ítem descríbese como Atribución-NoComercial-SinDerivadas 3.0 España
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- INIBIC-ICATC - Artigos [156]
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Specialized proresolving mediators protect against experimental autoimmune myocarditis by modulating Ca2+ handling and NRF2 activationAutor(es)
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2022-05-18Cita bibliográfica
Val-Blasco A, Prieto P, Íñigo Jaén R, Gil-Fernández M, Pajares M, Doménech N, et al. Specialized proresolving mediators protect against experimental autoimmune myocarditis by modulating Ca2+ handling and NRF2 activation. JACC Basic Transl Sci. 2022;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
Myocarditis
NRF2
Pro-resolving mediators
SERCA2A
Descrición
Preclinical research
Versión do editor
Dereitos
Atribución-NoComercial-SinDerivadas 3.0 España
ISSN
2452-302X
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