Key result
mAKAPβ scaffolds a cardiac myocyte signalosome to modulate stress genes and control pathological hypertrophy.
mAKAPβ acts as a critical scaffold protein in cardiac myocytes, integrating multiple signaling pathways to regulate gene expression involved in pathological cardiac hypertrophy.
Targeting mAKAPβ may mitigate hypertrophy; leaves open clinical translation pending in vivo validation.
Cardiac remodeling is regulated by an extensive intracellular signal transduction network. Each of the many signaling pathways in this network contributes uniquely to the control of cellular adaptation. In the last few years, it has become apparent that multimolecular signaling complexes or "signalosomes" are important for fidelity in intracellular signaling and for mediating crosstalk between the different signaling pathways. These complexes integrate upstream signals and control downstream effectors. In the cardiac myocyte, the protein mAKAPβ serves as a scaffold for a large signalosome that is responsive to cAMP, calcium, hypoxia, and mitogen-activated protein kinase signaling. The main function of mAKAPβ signalosomes is to modulate stress-related gene expression regulated by the transcription factors NFATc, MEF2, and HIF-1α and type II histone deacetylases that control pathological cardiac hypertrophy.
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Passariello et al. (2014) conducted a review in Cardiac remodeling. mAKAPβ was evaluated. The protein mAKAPβ serves as a scaffold for a large signalosome in cardiac myocytes, modulating stress-related gene expression to control pathological cardiac hypertrophy.
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