Key result
BML-111 prevents cardiac dysfunction and tissue damage in experimental autoimmune myocarditis by activating NRF2 signaling and preventing Ca2+ mishandling.
Why the study?
Does BML-111 prevent cardiac dysfunction and tissue damage in experimental autoimmune myocarditis?
Does BML-111 prevent cardiac dysfunction and tissue damage in experimental autoimmune myocarditis?
BML-111 shows potential as a therapeutic tool to prevent cardiac dysfunction in myocarditis by modulating NRF2 signaling and calcium handling.
Hypothesis-generating for BML-111 in myocarditis; human trials needed before clinical consideration.
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.
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Val‐Blasco et al. (2022) studied Experimental Autoimmune Myocarditis. 5(S), (6)R, 7-trihydroxyheptanoic acid methyl ester (BML-111) was evaluated on Cardiac dysfunction and tissue damage. BML-111 prevents cardiac dysfunction and tissue damage in experimental autoimmune myocarditis by activating NRF2 signaling and preventing Ca2+ mishandling.
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