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.

中文翻译：

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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。

成年哺乳动物心脏在心肌损伤后无法再生，因为大多数心肌细胞缺乏增殖能力。相比之下，脊椎动物的心肌细胞，如斑马鱼和 urodele 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，因此支持受损组织的再生和心脏功能的恢复。是否存在进化上保守的心肌细胞增殖调节机制，如果存在，它们是否可以修改以允许成年哺乳动物的心脏再生，这些都是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已成为脊椎动物心肌细胞周期和心脏再生的关键调节因子。在本次审查中，