Fig 12.

Model illustrating the role of the AKAP-Lbc/p38 activation complex in the regulation of compensatory cardiac hypertrophy. AKAP-Lbc assembles a signaling complex, which includes the scaffolding protein PKNα, as well as MLTK, MKK3, and p38α. In response to pressure overload, AKAP-Lbc promotes the formation of RhoA-GTP, which in turn induces the sequential activation of PKNα, MLTK, MKK3, and p38α within the AKAP-Lbc complex. This results in the activation of the mTOR signaling pathway that controls protein synthesis and promotes compensatory cardiac hypertrophy, which temporarily preserves the function of the stressed heart.