Fig. 5: A graphical study summary showing increased beneficial PLN ASO treatment effects with increased contribution of PLN to disease.

Summary figure of study results. Three murine models of a dilated cardiomyopathy were studied, including the genetically engineered mouse models of PLN R14^Δ/Δ and Csrp3/Mlp^−/−, and the rat myocardial infarction model. PLN functional defects are causative to the pathology observed in PLN R14^Δ/Δ, early contributing to the pathology in Csrp3/Mlp^−/−, and consequential and aggravating in myocardial infarction. In line with this, the beneficial effects of the PLN-ASO were most abundant in the PLN R14^Δ/Δ and Csrp3/Mlp^−/− models, showing almost complete prevention or reversal of disease phenotype. In our myocardial infarction model, the PLN-ASO restored cardiac dimensions and contractility, but not relaxation or left ventricular ejection fraction. ASO antisense oligonucleotide, ANP atrial natriuretic peptide.