宿敵オニール
Akt1 in the cardiovascular system: friend or foe?
Brian T. O’Neill and E. Dale Abel
Division of Endocrinology, Metabolism and Diabetes and Program in Human Molecular Biology and Genetics, University of Utah School of Medicine, Salt Lake City, Utah, USA.
Address correspondence to: E. Dale Abel, Division of Endocrinology, Metabolism and Diabetes, Program in Human Molecular Biology and Genetics, 15 North 2030 East, Building 533 Room 3410B, Salt Lake City, Utah 84112, USA. Phone: (801) 585-0727; Fax: (801) 585-0701; E-mail: dale.abel@hmbg.utah.edu.
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.
Aktを見えるようにしてみせよう，ホトトギス。
Akt1 in the cardiovascular system: friend or foe?
Brian T. O’Neill and E. Dale Abel
Division of Endocrinology, Metabolism and Diabetes and Program in Human Molecular Biology and Genetics, University of Utah School of Medicine, Salt Lake City, Utah, USA.
Address correspondence to: E. Dale Abel, Division of Endocrinology, Metabolism and Diabetes, Program in Human Molecular Biology and Genetics, 15 North 2030 East, Building 533 Room 3410B, Salt Lake City, Utah 84112, USA. Phone: (801) 585-0727; Fax: (801) 585-0701; E-mail: dale.abel@hmbg.utah.edu.
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.
Aktを見えるようにしてみせよう，ホトトギス。
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