mmi-0100 and Cardiomyopathies

mmi-0100 has been researched along with Cardiomyopathies* in 1 studies

Other Studies

1 other study(ies) available for mmi-0100 and Cardiomyopathies

ArticleYear
MMI-0100 Inhibits Cardiac Fibrosis in a Mouse Model Overexpressing Cardiac Myosin Binding Protein C.
    Journal of the American Heart Association, 2017, Sep-04, Volume: 6, Issue:9

    Cardiac stress can trigger production of a 40-kDa peptide fragment derived from the amino terminus of the cardiac myosin-binding protein C. Cardiac stress, as well as cMyBP-C mutations, can trigger production of 1 such truncated protein fragment, a 40-kDa peptide fragment derived from the amino terminus of cMyBP-C. Genetic expression of this 40-kDa fragment in mouse cardiomyocytes (cMyBP-C. Nontransgenic and cMyBP-C. Pharmaceutical inhibition of mitogen-activated protein kinase--activated protein kinase-2 signaling via MMI-0100 treatment is beneficial in the context of fibrotic cMyBPC

    Topics: Actins; Animals; Cardiomyopathies; Carrier Proteins; Cell Differentiation; Cells, Cultured; Disease Models, Animal; Fibroblasts; Fibrosis; Hypertrophy, Left Ventricular; Intracellular Signaling Peptides and Proteins; Mice, Inbred C57BL; Mice, Transgenic; Myocytes, Cardiac; Peptides; Protein Kinase Inhibitors; Protein Serine-Threonine Kinases; Up-Regulation; Ventricular Remodeling

2017