Cardioprotective responses to aerobic exercise-induced physiological hypertrophy in zebrafish heart.

IF 4.6 Q2 MATERIALS SCIENCE, BIOMATERIALS
Zhanglin Chen, Zuoqiong Zhou, Xiyang Peng, Chenchen Sun, Dong Yang, Chengli Li, Runkang Zhu, Ping Zhang, Lan Zheng, Changfa Tang
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引用次数: 7

Abstract

Herein, we aimed to establish an aerobic exercise-induced physiological myocardial hypertrophy zebrafish (Danio rerio) model and to explore the underlying molecular mechanism. After 4 weeks of aerobic exercise, the AMR and Ucrit of the zebrafish increased and the hearts were enlarged, with thickened myocardium, an increased number of myofilament attachment points in the Z-line, and increased compaction of mitochondrial cristae. We also found that the mTOR signaling pathway, angiogenesis, mitochondrial fusion, and fission event, and mitochondrial autophagy were associated with the adaptive changes in the heart during training. In addition, the increased mRNA expression of genes related to fatty acid oxidation and antioxidation suggested that the switch of energy metabolism and the maintenance of mitochondrial homeostasis induced cardiac physiological changes. Therefore, the zebrafish heart physiological hypertrophy model constructed in this study can be helpful in investigating the cardioprotective mechanisms in response to aerobic exercise.

有氧运动诱发斑马鱼心脏生理性肥大的心脏保护反应
在此,我们旨在建立有氧运动诱导生理性心肌肥厚的斑马鱼(Danio rerio)模型,并探索其潜在的分子机制。经过4周的有氧运动后,斑马鱼的AMR和Ucrit增加,心脏增大,心肌增厚,Z线的肌丝附着点增加,线粒体嵴压实增加。我们还发现,mTOR 信号通路、血管生成、线粒体融合和裂变事件以及线粒体自噬与训练期间心脏的适应性变化有关。此外,脂肪酸氧化和抗氧化相关基因的 mRNA 表达增加表明,能量代谢的转换和线粒体平衡的维持诱导了心脏生理变化。因此,本研究构建的斑马鱼心脏生理性肥大模型有助于研究有氧运动的心脏保护机制。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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来源期刊
ACS Applied Bio Materials
ACS Applied Bio Materials Chemistry-Chemistry (all)
CiteScore
9.40
自引率
2.10%
发文量
464
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