The mammalian fetal heart relies primarily on glucose and pyruvate as substrates for ATP production, and it is rapidly transformed to fatty acid β-oxidation (FAO) postnatally. However, energy metabolic pathways rever...The mammalian fetal heart relies primarily on glucose and pyruvate as substrates for ATP production, and it is rapidly transformed to fatty acid β-oxidation (FAO) postnatally. However, energy metabolic pathways revert to a fetal pattern, when cardiac hypertrophy and heart failure developed. This return was called recapitulation, ultimately it is maladaptive for the body. The process of FAO was performed under a precise regulating system, nuclear transcription factors such as PPARα, Sp1/3, Coup-TF(chicken ovalbumin upstream promoter transcription factor) all take part in the regulation of genes transcription of FAO enzymes. It was identified that the reguction of PPARα activity in hypertrophic myocardium due to pressure overload might result in down-regulation of gene expression of FAO enzyme. The mechanism involved in reinduction of a fetal gene transcription participated in the regulation of myocardial energy metabolism in the development of cardiac hypertrophy resulting from pressure overload.展开更多
文摘The mammalian fetal heart relies primarily on glucose and pyruvate as substrates for ATP production, and it is rapidly transformed to fatty acid β-oxidation (FAO) postnatally. However, energy metabolic pathways revert to a fetal pattern, when cardiac hypertrophy and heart failure developed. This return was called recapitulation, ultimately it is maladaptive for the body. The process of FAO was performed under a precise regulating system, nuclear transcription factors such as PPARα, Sp1/3, Coup-TF(chicken ovalbumin upstream promoter transcription factor) all take part in the regulation of genes transcription of FAO enzymes. It was identified that the reguction of PPARα activity in hypertrophic myocardium due to pressure overload might result in down-regulation of gene expression of FAO enzyme. The mechanism involved in reinduction of a fetal gene transcription participated in the regulation of myocardial energy metabolism in the development of cardiac hypertrophy resulting from pressure overload.
