Metabolic regulation of cardiac regeneration: roles of hypoxia, energy homeostasis, and mitochondrial dynamics
Metabolic regulation of cardiac regeneration: roles of hypoxia, energy homeostasis, and mitochondrial dynamics
复制标题
心脏再生的代谢调节：缺氧、能量稳态和线粒体动力学的作用
DOI：
10.1016/j.gde.2021.05.009
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发表时间：
2021
影响因子：
4
通讯作者：
Kimura Wataru
中科院分区：
文献类型：
--
作者：
Sakaguchi Akane;Kimura Wataru
成年哺乳动物心脏在心肌损伤后不能再生，因为大多数心肌细胞缺乏增殖能力。相反，脊椎动物（如斑马鱼和尾纲两栖动物）以及胎儿和早期新生哺乳动物的心肌细胞保持增殖能力，从而支持损伤组织的再生和心功能的恢复。心肌细胞增殖的进化保守调节机制是否存在，如果存在，它们是否可以被修改以允许成年哺乳动物的心脏再生，这是一个具有重大科学和医学意义的问题。环境缺氧、缺氧诱导的细胞信号传导和线粒体代谢最近被认为是脊椎动物心肌细胞周期和心脏再生的关键调节因子。在这篇综述中，我们讨论了几种模型动物的心脏再生能力，并讨论了与缺氧和线粒体代谢相关的诱导治疗性心脏再生的潜在策略。
The adult mammalian heart cannot regenerate after myocardial injury because most cardiomyocytes lack the ability to proliferate. In contrast, cardiomyocytes of vertebrates such as zebrafish and urodele amphibians, but also those of fetal and early neonatal mammals, maintain the ability to proliferate and therefore support regeneration of injured tissue and recovery of cardiac function. Whether evolutionarily conserved regulatory mechanisms of cardiomyocyte proliferation exist and, if so, whether they are modifiable to allow cardiac regeneration in adult mammals are questions of great scientific and medical interest. Environmental hypoxia, hypoxia-induced cellular signaling, and mitochondrial metabolism have recently emerged as key regulators of the cardiomyocyte cell cycle and cardiac regeneration in vertebrates. In this review, we address the cardiac regenerative capacity of several model animals and discuss potential strategies related to hypoxia and mitochondrial metabolism for induction of therapeutic heart regeneration.