Fig. 6From: Forced expression of miR-143 and -145 in cardiomyocytes induces cardiomyopathy with a reductive redox shiftSchematic depiction of the signaling cascade in αMHC/miR-143/145TG mice. A hypothetical signaling model for a reductive state in αMHC/miR-143/145TG mice is shown. Our data indicate that the overexpression of miR-143 plays a pivotal role in the pathogenesis of the αMHC/miR-143/145TG phenotype, but the key targets for miR-143 triggering this process have not been identified and are shown with a question mark. *: Although the expression of HK2 was suppressed in transgenic hearts, in vitro HK activity was comparable in the L9 and NTG mouse hearts. Since the expression levels of GR, γ-GCSC, p62 and G6PD are controlled by Nrf2, these four molecules are surrounded by a red box. A detailed explanation is given in the Discussion sectionBack to article page