Tian Rong
Department of Medicine, NMR Laboratory for Physiological Chemistry, Brigham and Women's Hospital and Harvard Medical School, Boston, MA 02115, USA.
Curr Hypertens Rep. 2003 Dec;5(6):454-8. doi: 10.1007/s11906-003-0052-7.
Impaired myocardial energy metabolism in cardiac hypertrophy and failure is characterized by decreased fatty-acid oxidation and increased glucose utilization. Mechanisms involving deactivation of peroxisome proliferator-activated receptor alpha/relinoid X receptor alpha (PPARalpha/RXRalpha),and activation of chicken ovalbumin upstream promoter transcription factor (COUP-TF), and transcription factors Sp1 and Sp3, lead to decreased capacity for fatty acid utilization in hypertrophied hearts. Furthermore, impaired myocardial energetic status stimulates glucose uptake and glycolysis, which, in combination with the permissive effect due to decreased fatty acid oxidation, promotes increases in glucose utilization in hypertrophied hearts. Finally, shifting substrate utilization toward glucose is likely adaptive and has the potential to delay transition to heart failure.
心肌肥厚和心力衰竭时心肌能量代谢受损的特征是脂肪酸氧化减少和葡萄糖利用增加。涉及过氧化物酶体增殖物激活受体α/类视黄醇X受体α（PPARα/RXRα）失活、鸡卵清蛋白上游启动子转录因子（COUP-TF）激活以及转录因子Sp1和Sp3的机制，导致肥厚心肌中脂肪酸利用能力下降。此外，心肌能量状态受损会刺激葡萄糖摄取和糖酵解，这与脂肪酸氧化减少所产生的允许作用相结合，促进了肥厚心肌中葡萄糖利用的增加。最后，将底物利用转向葡萄糖可能具有适应性，并有可能延迟向心力衰竭的转变。
