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In addition, the potential of genotype-specific therapeutic approaches has been explored: in genetic murine LQT3 models, with pathologically enhanced late I Na , sodium-channel blockers mexiletine, flecainide and the more selective GS967 exert a mechanism-directed, genotype-specific antiarrhythmic effect [38,39,40]

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Degradation of lipid droplet-associated proteins by chaperone-mediated autophagy facilitates lipolysis

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