心血管系统中的Akt1：是友还是敌？
Akt1 in the cardiovascular system: friend or foe?
作者信息
O'Neill Brian T, Abel E Dale
机构信息
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.
出版信息
J Clin Invest. 2005 Aug;115(8):2059-64. doi: 10.1172/JCI25900.
Abstract
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.
摘要
Akt是一种重要的信号分子，可调节许多细胞过程，如细胞生长、存活和代谢。Akt激活已被提议作为增加缺血后心肌细胞存活的潜在策略。在哺乳动物细胞中，存在3种不同的Akt亚型，但它们在心血管生物学中的精确作用此前尚不清楚。本期《临床研究杂志》发表的三项独立研究，现在为Akt1在血管生成调节中的核心作用以及心脏中慢性不受调控的Akt激活的不良或有害后果提供了重要的新见解（见第2108、2119和2128页开始的相关文章）。在此我们讨论这些令人兴奋的新研究的意义。
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1
Akt1 in the cardiovascular system: friend or foe?心血管系统中的Akt1：是友还是敌？
J Clin Invest. 2005 Aug;115(8):2059-64. doi: 10.1172/JCI25900.
2
Disruption of coordinated cardiac hypertrophy and angiogenesis contributes to the transition to heart failure.协调性心脏肥大和血管生成的破坏促成了向心力衰竭的转变。
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Akt1/protein kinase Balpha is critical for ischemic and VEGF-mediated angiogenesis.Akt1/蛋白激酶Bα对缺血和VEGF介导的血管生成至关重要。
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Akt3 overexpression in the heart results in progression from adaptive to maladaptive hypertrophy.心脏中Akt3的过表达会导致从适应性肥大向病理性肥大的进展。
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本文引用的文献
1
Akt1/protein kinase Balpha is critical for ischemic and VEGF-mediated angiogenesis.Akt1/蛋白激酶Bα对缺血和VEGF介导的血管生成至关重要。
J Clin Invest. 2005 Aug;115(8):2119-27. doi: 10.1172/JCI24726.
2
Disruption of coordinated cardiac hypertrophy and angiogenesis contributes to the transition to heart failure.协调性心脏肥大和血管生成的破坏促成了向心力衰竭的转变。
J Clin Invest. 2005 Aug;115(8):2108-18. doi: 10.1172/JCI24682.
3
PI3K rescues the detrimental effects of chronic Akt activation in the heart during ischemia/reperfusion injury.磷脂酰肌醇-3激酶可挽救缺血/再灌注损伤期间心脏中慢性Akt激活的有害影响。
J Clin Invest. 2005 Aug;115(8):2128-38. doi: 10.1172/JCI23073. Epub 2005 Jul 7.
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Paracrine action accounts for marked protection of ischemic heart by Akt-modified mesenchymal stem cells.旁分泌作用是Akt修饰的间充质干细胞对缺血性心脏产生显著保护作用的原因。
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Role for Akt3/protein kinase Bgamma in attainment of normal brain size.Akt3/蛋白激酶Bγ在实现正常脑容量中的作用。
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Akt mediates the cross-talk between beta-adrenergic and insulin receptors in neonatal cardiomyocytes.Akt介导新生心肌细胞中β-肾上腺素能受体与胰岛素受体之间的相互作用。
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Deletion of ribosomal S6 kinases does not attenuate pathological, physiological, or insulin-like growth factor 1 receptor-phosphoinositide 3-kinase-induced cardiac hypertrophy.核糖体S6激酶的缺失并不会减弱病理性、生理性或胰岛素样生长因子1受体-磷酸肌醇3激酶诱导的心脏肥大。
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