From the Max-Planck-Institute for Heart and Lung Research, Bad Nauheim, Germany (X.Y., T.B.); and Department of Internal Medicine II, Justus Liebig University Giessen, Member of the German Center for Cardiovascular Research (DZHK), Member of the German Center for Lung Research (DZL), Giessen, Germany (T.B.).
Circ Res. 2017 Jul 21;121(3):293-309. doi: 10.1161/CIRCRESAHA.117.308428.
Efficient cardiac regeneration is closely associated with the ability of cardiac myocytes to proliferate. Fetal or neonatal mouse hearts containing proliferating cardiac myocytes regenerate even extensive injuries, whereas adult hearts containing mostly post-mitotic cardiac myocytes have lost this ability. The same correlation is seen in some homoiotherm species such as teleost fish and urodelian amphibians leading to the hypothesis that cardiac myocyte proliferation is a major driver of heart regeneration. Although cardiomyocyte proliferation might not be the only prerequisite to restore full organ function after cardiac damage, induction of cardiac myocyte proliferation is an attractive therapeutic option to cure the injured heart and prevent heart failure. To (re)initiate cardiac myocyte proliferation in adult mammalian hearts, a thorough understanding of the molecular circuitry governing cardiac myocyte cell cycle regulation is required. Here, we review the current knowledge in the field focusing on the withdrawal of cardiac myocytes from the cell cycle during the transition from neonatal to adult stages.
有效的心脏再生与心肌细胞的增殖能力密切相关。含有增殖心肌细胞的胎儿或新生鼠心脏甚至可以再生广泛的损伤，而含有大多数有丝分裂后心肌细胞的成年心脏已经失去了这种能力。这种相关性在一些恒温动物物种中也存在，如硬骨鱼和有尾两栖动物，这导致了心肌细胞增殖是心脏再生的主要驱动因素的假说。尽管心肌细胞增殖可能不是心脏损伤后恢复完全器官功能的唯一前提条件，但诱导心肌细胞增殖是治疗受损心脏和预防心力衰竭的一种有吸引力的治疗选择。为了在成年哺乳动物心脏中（重新）启动心肌细胞增殖，需要深入了解控制心肌细胞细胞周期调控的分子机制。在这里，我们回顾了该领域的现有知识，重点介绍了从新生儿到成年阶段过渡过程中心肌细胞退出细胞周期的机制。
