> In our gold-standard mouse studies, the three proteins outperformed existing treatments.
These studies showed that the proteins successfully preserved left ventricular function compared to control treated animals at d15 post-MI, with significantly larger diastolic volume at d60 post-MI when heart failure occurs in controls.
There was no evidence of pathological remodelling in treated animals. As early as d2 post-MI the positive cellular effect of these proteins was observed to include prevention of cardiomyocyte apoptosis by TUNEL staining of heart tissue and removal of cellular damage by autophagy shown by LC3 positive autophagosomes and autophagic flux. Lastly, one of the proteins had a profound anti-fibrotic effect, preventing fibroblast activation and scarring through suppression of TGF-beta mediated pathology.