Key result
Mitochondrial AKAPs regulate cardiac cAMP signaling, emerging as potential therapeutic targets in cardiovascular disease.
This review highlights mitochondrial AKAPs as critical signaling hubs in the cardiovascular system and potential targets for therapeutic intervention in cardiac diseases.
Hypothesis-generating for mitochondrial AKAP modulation in cardiovascular disease; prospective trials needed before clinical adoption.
Second messenger cyclic adenosine monophosphate (cAMP) has been found to regulate multiple mitochondrial functions, including respiration, dynamics, reactive oxygen species production, cell survival and death through the activation of cAMP-dependent protein kinase A (PKA) and other effectors. Several members of the large family of A kinase anchor proteins (AKAPs) have been previously shown to locally amplify cAMP/PKA signaling to mitochondria, promoting the assembly of signalosomes, regulating multiple cardiac functions under both physiological and pathological conditions. In this review, we will discuss roles and regulation of major mitochondria-targeted AKAPs, along with opportunities and challenges to modulate their functions for translational purposes in the cardiovascular system.
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Paolillo et al. (2022) conducted a review in Cardiovascular diseases and mitochondrial function. Mitochondrial A kinase anchor proteins (AKAPs) was evaluated. Mitochondrial AKAPs amplify cAMP/PKA signaling to mitochondria and regulate multiple cardiac functions, representing novel potential targets for targeted therapy in cardiovascular diseases.
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