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Background  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 40k ) leads to cardiac disease, fibrosis, and death within the first year. Fibrosis can occur in many cardiovascular diseases, and mitogen‐activated protein kinase––activated protein kinase‐2 signaling has been implicated in a variety of fibrotic processes. Recent studies demonstrated that mitogen‐activated protein kinase––activated protein kinase‐2 inhibition using the cell‐permeant peptide inhibitor  MMI ‐0100 is protective in the setting of acute myocardial infarction. We hypothesized that  MMI ‐0100 might also be protective in a chronic model of fibrosis, produced as a result of  cMyBP ‐C 40k  cardiomyocyte expression.    Methods and Results  Nontransgenic and  cMyBP ‐C 40k  inducible transgenic mice were given  MMI ‐0100 or  PBS  daily for 30 weeks. In control groups, long‐term  MMI ‐0100 was benign, with no measurable effects on cardiac anatomy, function, cell viability, hypertrophy, or probability of survival. In the inducible transgenic group,  MMI ‐0100 treatment reduced cardiac fibrosis, decreased cardiac hypertrophy, and prolonged survival.    Conclusions  Pharmaceutical inhibition of mitogen‐activated protein kinase––activated protein kinase‐2 signaling via  MMI ‐0100 treatment is beneficial in the context of fibrotic  cMyBPC  40k  disease.

MMI ‐0100 Inhibits Cardiac Fibrosis in a Mouse Model Overexpressing Cardiac Myosin Binding Protein C