This review highlights the dual role of AKT signaling in the heart, where short-term activation is protective but long-term activation leads to pathological hypertrophy and heart failure.
Short-term AKT activation may confer cardiac protection; leaves open duration-specific targeting strategies pending clinical trials.
AKT is a serine/threonine protein kinase, also known as protein kinase B, which regulates cardiac growth, myocardial angiogenesis, glucose metabolism, and cell death in cardiac myocytes. AKT is activated by its phosphorylation at Thr 308 and ser 473 by PDK1 and mTORC2, respectively, in response to trophic stimuli such as insulin and insulin growth factor. c-Jun N-Terminal Kinases (JNKs) phosphorylate AKT at Thr 450 and potentiate its interaction with its downstream effectors. The short-term activation of AKT promotes physiological hypertrophy and protection from myocardial injury; whereas, its long-term activation causes pathological hypertrophy and heart failure. In this review we will discuss the role of AKT in regulating signalling pathways in the heart with special emphasis on the role of AKT in modulating stress induced autophagic cell death in cardiomyocytes in vitro.
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Chaanine et al. (2011) studied this question.
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