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首页> 外文期刊>Cell metabolism >A conserved role for phosphatidylinositol 3-kinase but not Akt signaling in mitochondrial adaptations that accompany physiological cardiac hypertrophy.
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A conserved role for phosphatidylinositol 3-kinase but not Akt signaling in mitochondrial adaptations that accompany physiological cardiac hypertrophy.

机译：在伴随生理性心肌肥大的线粒体适应中，磷脂酰肌醇3-激酶的保守作用而非Akt信号传导。

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Physiological cardiac hypertrophy is associated with mitochondrial adaptations that are characterized by activation of PGC-1alpha and increased fatty acid oxidative (FAO) capacity. It is widely accepted that phosphatidylinositol 3-kinase (PI3K) signaling to Akt1 is required for physiological cardiac growth. However, the signaling pathways that coordinate physiological hypertrophy and metabolic remodeling are incompletely understood. We show here that activation of PI3K is sufficient to increase myocardial FAO capacity and that inhibition of PI3K signaling prevents mitochondrial adaptations in response to physiological hypertrophic stimuli despite increased expression of PGC-1alpha. We also show that activation of the downstream kinase Akt is not required for the mitochondrial adaptations that are secondary to PI3K activation. Thus, in physiological cardiac growth, PI3K is an integrator of cellular growth and metabolic remodeling. Although PI3K signaling to Akt1 is required for cellular growth, Akt-independent pathways mediate the accompanying mitochondrial adaptations.
机译：生理性心脏肥大与线粒体适应有关，其特征在于PGC-1alpha的激活和脂肪酸氧化（FAO）能力的增强。生理心脏生长需要信号传导至Akt1的磷脂酰肌醇3-激酶（PI3K）。但是，协调生理肥大和代谢重塑的信号通路尚不完全了解。我们在这里显示PI3K的激活足以增加心肌的FAO能力，并且尽管PGC-1alpha的表达增加，但PI3K信号的抑制作用阻止了线粒体适应生理性肥厚刺激。我们还显示，对于继发于PI3K激活的线粒体适应而言，下游激酶Akt的激活不是必需的。因此，在生理性心脏生长中，PI3K是细胞生长和代谢重塑的整合者。虽然PI3K信号转导Akt1是细胞生长所必需的，但Akt依赖性途径可介导伴随的线粒体适应。

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