Specialized Proresolving Mediators Protect Against Experimental Autoimmune Myocarditis by Modulating Ca2+ Handling and NRF2 Activation.
Abstract: Highlights
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Administration of BML-111, a stable LXA4 analog, protects against cardiac dysfunction by avoiding Ca2+ mishandling induced by autoimmune myocarditis in a mouse model.
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Beneficial effects of the SPMs on intracellular Ca2+ handling are mainly caused by a regulation of SERCA2A by NRF2.
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Cardiac tissue obtained from individuals diagnosed with myocarditis, compared with healthy myocardium tissues, displayed depressed mRNA levels of ATP2A2 (SERCA2A) and NF2L2 (NRF2).
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