RNF207 exacerbates pathological cardiac hypertrophy via post-translational modification of TAB1.

There is currently a lack of treatment to effectively prevent or reverse cardiac hypertrophy and heart failure, which has brought the importance of in-depth understanding of the molecular mechanisms that drives the pathological cardiac growth and the discovery of novel therapeutic targets. Our work demonstrates for the first time that RNF207 exaggerates pressure overload-induced cardiac hypertrophy and dysfunction. This is due, at least in part, to the polyubiquitination of TAB1, which triggers the autophosphorylation of TAK1 and activation of TAK1-p38 and TAK1-JNK1/2 signaling pathways. These data suggest that RNF207 may be a potential therapeutic target in the treatment of cardiac hypertrophy and failure.