Key result
A-kinase anchor proteins (AKAPs) play diverse pro- and anti-hypertrophic roles in the heart by forming signaling complexes that integrate multiple pathways.
AKAPs serve as critical molecular scaffolds in the heart, integrating multiple signaling pathways that regulate cardiac hypertrophy.
May guide scaffold-targeted therapies for hypertrophy; leaves open validation of specific complexes in trials.
Originally identified as mediators of cyclic adenosine monophosphate (cAMP) and protein kinase A signaling, A-kinase anchor proteins (AKAPs) are now recognized as a diverse family of molecular scaffolds capable of interacting with many other proteins. Members of the AKAP family within the heart can take on either pro- or anti-hypertrophic roles by interacting with a myriad of protein kinases and phosphatases in the process. AKAPs often form the core of large signaling complexes (or signalosomes) that allow multiple pathways to converge and functionally intertwine. Approximately 30% of AKAPs discovered to date are expressed in the heart, but the functions of many of these remain to be discovered. This review focuses on AKAPs that have been demonstrated to play roles in mediating cardiac hypertrophy.
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Blant et al. (2012) conducted a review in Cardiac hypertrophy. A-kinase anchor proteins (AKAPs) was evaluated. A-kinase anchor proteins (AKAPs) play diverse pro- and anti-hypertrophic roles in the heart by forming signaling complexes that integrate multiple pathways.
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