Department of Pediatrics, University of Cincinnati, Cincinnati Children's Hospital Medical Center, Cincinnati, Ohio 45229, USA.
Nat Rev Mol Cell Biol. 2013 Jan;14(1):38-48. doi: 10.1038/nrm3495.
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.
心脏会对发育信号和增加的工作量做出反应而发生肥大。尽管成年后发生的心肌肥厚最终可能导致疾病，但心肌肥厚不一定是适应不良的，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有了更多的了解。生理性心肌肥厚是由有限的信号启动的，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，它们汇聚到有限数量的细胞内信号通路（如 PI3K、AKT、AMP 激活蛋白激酶和 mTOR）上，从而影响基因转录、蛋白质翻译和代谢。利用适应性信号介质来重振患病心脏可能具有重要的医学意义。
