microRNA-132

Human cardiac tissue miR-132 concentrations were not measured in the trial. Circulating miR-132 may not directly represent myocardial tissue miR-132 levels. Preclinical inhibition of miR-132 halted or partly reversed pathological remodeling in heart failure models. The trial rationale was based on miR-132 being upregulated after myocardial stress and regulating pathological cardiac remodeling. miR-132 has been linked to cardiomyocyte hypertrophy, impaired calcium handling, impaired contractility, myocardial fibrosis, and reduced autophagy regulation. Plasma miR-132 partly rebounded after treatment stopped, especially in the lower-dose group. Plasma miR-132 was used as a pharmacodynamic marker in the trial.