Skip to main content
. Author manuscript; available in PMC: 2021 Dec 1.
Published in final edited form as: Circulation. 2020 Sep 16;142(22):2138–2154. doi: 10.1161/CIRCULATIONAHA.119.044805

Figure 8. Model for the role of SRF S103 phosphorylation in the regulation of pathological cardiac hypertrophy.

Figure 8.

Increased width and length of the cardiac myocyte results in increased ventricular (LV – left, RV – right) wall thickness and internal diameter in pathological concentric and eccentric hypertrophy, respectively, ultimately leading to heart failure.2 Depending upon the pathophysiologic condition, pressure overloaded hearts can undergo ventricular dilation, resulting in a ventricle like in eccentric hypertrophy. The RSK3 anchoring disruptor peptide RBD, that displaces RSK3 from mAKAPβ signalosomes, will inhibit SRF phosphorylation and concentric hypertrophy. The PP2A anchoring disruptor PBD, that displaces PP2A from mAKAPβ signalosomes, will promote SRF phosphorylation and inhibit ventricular dilation and eccentric hypertrophy.