Transcriptional regulation of energy substrate metabolism in normal and hypertrophied heart

被引：38

作者：

Tian, R

机构：

[1] Brigham & Womens Hosp, Dept Med, NMR Lab Physiol Chem, Boston, MA 02115 USA

[2] Harvard Univ, Sch Med, Boston, MA 02115 USA

来源：

CURRENT HYPERTENSION REPORTS | 2003年 / 5卷 / 06期

关键词：

D O I：

10.1007/s11906-003-0052-7

中图分类号：

R6 [外科学];

学科分类号：

1002 ; 100210 ;

摘要：

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.

引用

收藏

页码：454 / 458

页数：5

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