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首页> 外文期刊>Hypertension: An Official Journal of the American Heart Association >Peroxisome Proliferator-Activated Receptor β/δ Activation in Adult Hearts Facilitates Mitochondrial Function and Cardiac Performance Under Pressure-Overload Condition
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Peroxisome Proliferator-Activated Receptor β/δ Activation in Adult Hearts Facilitates Mitochondrial Function and Cardiac Performance Under Pressure-Overload Condition

机译：成年心脏中过氧化物酶体增殖物激活的受体β/δ激活促进压力超负荷条件下的线粒体功能和心脏功能

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Peroxisome proliferator-activated receptor β/δ (PPARβ/δ) is an essential transcription factor in myocardial metabolism. This study aims to investigate the effects of PPARβ/δ activation in the adult heart on mitochondrial biology and oxidative metabolism under normal and pressure-overload conditions. We have investigated the effects of cardiac constitutively active PPARβ/δ in adult mice using a tamoxifen-inducible transgenic approach with Cre-LoxP recombination. The expression of PPARβ/δ mRNA and protein in cardiomyocytes of adult mice was substantially increased after short-term induction. In these mice, the cardiac expression of key factors involved in mitochondrial biogenesis, such as PPARγ coactivator-1, endogenous antioxidants Cu/Zn superoxide dismutase, and catalase, fatty acid, and glucose metabolism, such as carnitine palmitoyltransferase Ib, carnitine palmitoyltransferase II, and glucose transporter 4, were upregulated. Subsequently, myocardial oxidative metabolism was elevated concomitant with an increased mitochondrial DNA copy number and an enhanced cardiac performance. Moreover, activation of PPARβ/δ in the adult heart improved cardiac function and resisted progression to pathological development in mechanical stress condition. We conclude that PPARβ/δ activation in the adult heart will promote cardiac performance along with transcriptional upregulation of mitochondrial biogenesis and defense, as well as oxidative metabolism at basal and pressure-overload conditions.
机译：过氧化物酶体增殖物激活受体β/δ（PPARβ/δ）是心肌代谢中必不可少的转录因子。本研究旨在研究正常和压力超负荷条件下成年心脏中PPARβ/δ活化对线粒体生物学和氧化代谢的影响。我们已经研究了他莫昔芬诱导的转基因方法与Cre-LoxP重组对成年小鼠心脏组成活性PPARβ/δ的影响。短期诱导后，成年小鼠心肌细胞中PPARβ/δmRNA和蛋白的表达明显增加。在这些小鼠中，与线粒体生物发生有关的关键因子的心脏表达，例如PPARγcoactivator-1，内源性抗氧化剂Cu / Zn超氧化物歧化酶，以及过氧化氢酶，脂肪酸和葡萄糖代谢，例如肉碱棕榈酰转移酶Ib，肉碱棕榈酰转移酶II，和葡萄糖转运蛋白4，被上调。随后，心肌氧化代谢增加，同时线粒体DNA拷贝数增加，心脏性能增强。此外，成年心脏中PPARβ/δ的活化改善了心脏功能，并在机械应激条件下抵抗了病理发展。我们得出的结论是，成年心脏中的PPARβ/δ激活将促进心脏功能以及线粒体生物发生和防御的转录上调以及在基础和压力超负荷条件下的氧化代谢。

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