Abstract
Introduction: Despite the improvements made in cardiac patient treatment and outcomes, current therapies only serve to alleviate the symptoms of cardiac fibrosis, rather than treat the disease itself. Our lab has previously established Ski as a potent inhibitor of TGF-β signalling in cardiac myofibroblasts, the primary effectors of fibrosis; however our recent investigations suggest that Ski may inhibit a multitude of pro-fibrotic pathways, including Hippo. To further expand the current knowledge on Ski's anti-fibrotic properties, and provide insight into potential mechanisms of action, we mapped its interactome using enzyme-catalyzed biotin proximity labelling (BioID2).
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