Allard Michael F
The James Hogg iCapture Centre for Cardiovascular and Pulmonary Research, Room 166, St. Pauls Hospital, 1081 Burrard Street, Vancouver, BC, Canada.
Curr Hypertens Rep. 2004 Dec;6(6):430-5. doi: 10.1007/s11906-004-0036-2.
Cardiac hypertrophy is a response to long-term pathologic (eg, hypertension) or physiologic (eg, exercise) hemodynamic overload accompanied by changes in energy substrate utilization. The pattern of substrate utilization (or metabolic phenotype) differs dramatically between pathologic and physiologic cardiac hypertrophy with directionally opposite changes in oxidation of fatty acids and glucose and glycolysis. These findings indicate that the metabolic response to long-term alterations in hemodynamic workload is not stereotypical, but is influenced by the nature of the stimulus leading to cardiac hypertrophy. Although the changes in substrate utilization are adaptive, in the case of pathologic stimuli, the changes in metabolism interfere with functional resiliency of the heart to metabolic stress, as occurs during ischemia-reperfusion. The distinct metabolic phenotypes of hearts hypertrophied in response to pathologic or physiologic stimuli are due not only to alteration in expression of metabolic enzymes and proteins, but also to post-translational modulation of metabolic enzymes and proteins.
心脏肥大是对长期病理性（如高血压）或生理性（如运动）血流动力学过载的一种反应，伴有能量底物利用的变化。病理性和生理性心脏肥大之间底物利用模式（或代谢表型）显著不同，脂肪酸和葡萄糖氧化以及糖酵解发生方向相反的变化。这些发现表明，对长期血流动力学负荷改变的代谢反应并非千篇一律，而是受导致心脏肥大的刺激性质影响。尽管底物利用的变化具有适应性，但在病理性刺激的情况下，代谢变化会干扰心脏对代谢应激的功能弹性，如在缺血再灌注期间发生的那样。因病理性或生理性刺激而肥大的心脏具有不同的代谢表型，这不仅归因于代谢酶和蛋白质表达的改变，还归因于代谢酶和蛋白质的翻译后调节。
