PI3K isoforms play distinct roles in cardiac hypertrophy and failure, acting through both kinase activity and protein-protein interactions.
Signal transduction events are key modulators of cellular function and, in the cardiovascular system, an emerging role is played by phosphoinositide 3-kinases (PI3Ks), a family of enzymes containing a 3-phosphorylated phosphoinositide that produce lipid second messengers. In the heart, multiple PI3K isoforms are expressed, but play potentially distinct roles. Among cardiac PI3Ks, PI3Kalpha is triggered by tyrosine kinase receptors and plays a role in adaptive hypertrophy, while PI3Kgamma is triggered by G protein-coupled receptors and is involved in maladaptive heart remodeling. This view has been recently complicated by the finding that PI3Ks can also be involved in protein-protein interactions and affect signaling independently of their kinase activity. This review will thus focus on the effects of these multiple signaling events, with particular emphasis on their involvement in cardiac hypertrophy and failure.
Damilano et al. (Mon,) conducted a review in Cardiac hypertrophy and failure. PI3K signaling was evaluated. PI3K isoforms play distinct roles in cardiac hypertrophy and failure, acting through both kinase activity and protein-protein interactions.
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