Akt1 in the cardiovascular system: friend or foe?
Akt is an important signaling molecule that modulates many cellular processes such as cell growth, survival, and metabolism. Akt activation has been proposed as a potential strategy for increasing cardiomyocyte survival following ischemia. In mammalian cells, 3 distinct isoforms of Akt exist, but their precise roles in cardiovascular biology were previously unknown. Three separate studies published in this issue of the JCI now provide important new insight into the central role of Akt1 in the regulation of angiogenesis and the maladaptive or deleterious consequences of chronic unregulated Akt activation in the heart (see the related articles beginning on pages 2108, 2119, and 2128). Here we discuss the implications of these exciting new studies.
O'Neill
Brian T
BT
Division of Endocrinology, Metabolism and Diabetes and Program in Human Molecular Biology and Genetics, University of Utah School of Medicine, Salt Lake City, Utah 84112, USA.
Abel
E Dale
ED
D000818:Animals; D002470:Cell Survival; D004789:Enzyme Activation; D006321:Heart; D006801:Humans; D007527:Isoenzymes / Q000378:metabolism; D017202:Myocardial Ischemia / Q000201:enzymology* / Q000473:pathology; D009206:Myocardium / Q000201:enzymology* / Q000473:pathology; D032383:Myocytes, Cardiac / Q000378:metabolism* / Q000473:pathology; D009389:Neovascularization, Pathologic / Q000201:enzymology*; D017346:Protein Serine-Threonine Kinases / Q000378:metabolism*; D011518:Proto-Oncogene Proteins / Q000378:metabolism*; D051057:Proto-Oncogene Proteins c-akt
D007527:Isoenzymes; D011518:Proto-Oncogene Proteins; C494918:AKT1 protein, human; D017346:Protein Serine-Threonine Kinases; D051057:Proto-Oncogene Proteins c-akt