Molecular basis of physiological heart growth: fundamental concepts and new players.
Molecular basis of physiological heart growth: fundamental concepts and new players.
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DOI：
10.1038/nrm3495
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发表时间：
2013-01
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影响因子：
--
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中科院分区：
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--
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心脏肥大是对发育信号和工作量增加的反应。虽然成人心肌肥厚最终可能导致疾病，但心肌肥厚并不一定是适应性不良，甚至可能是有益的。我们对生理性心肌肥厚的结构和分子特征，以及调节它的内分泌效应物和相关信号通路的理解取得了进展。生理性肥大是由有限的信号引发的，这些信号包括生长激素（如甲状腺激素、胰岛素、胰岛素样生长因子1和血管内皮生长因子）和机械力，它们汇聚在有限数量的细胞内信号通路（如PI3K、AKT、amp激活的蛋白激酶和mTOR）上，影响基因转录、蛋白质翻译和代谢。利用适应性信号介质使患病的心脏恢复活力可能具有重要的医学意义。
The heart hypertrophies in response to developmental signals as well as increased workload. Although adult-onset hypertrophy can ultimately lead to disease, cardiac hypertrophy is not necessarily maladaptive and can even be beneficial. Progress has been made in our understanding of the structural and molecular characteristics of physiological cardiac hypertrophy, as well as of the endocrine effectors and associated signalling pathways that regulate it. Physiological hypertrophy is initiated by finite signals, which include growth hormones (such as thyroid hormone, insulin, insulin-like growth factor 1 and vascular endothelial growth factor) and mechanical forces that converge on a limited number of intracellular signalling pathways (such as PI3K, AKT, AMP-activated protein kinase and mTOR) to affect gene transcription, protein translation and metabolism. Harnessing adaptive signalling mediators to reinvigorate the diseased heart could have important medical ramifications.
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Bueno, OF;De Windt, LJ;Molkentin, JD
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Boström P;Mann N;Wu J;Quintero PA;Plovie ER;Panáková D;Gupta RK;Xiao C;MacRae CA;Rosenzweig A;Spiegelman BM
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