心肌可塑性：心脏发育、再生与疾病
Myocardial plasticity: cardiac development, regeneration and disease.
作者信息
Bloomekatz Joshua, Galvez-Santisteban Manuel, Chi Neil C
机构信息
Department of Medicine, Division of Cardiology, University of California, San Diego, La Jolla, CA 92093, USA.
Department of Medicine, Division of Cardiology, University of California, San Diego, La Jolla, CA 92093, USA; Institute of Genomic Medicine, University of California, San Diego, La Jolla, CA 92093, USA.
出版信息
Curr Opin Genet Dev. 2016 Oct;40:120-130. doi: 10.1016/j.gde.2016.05.029. Epub 2016 Aug 4.
The adult mammalian heart is unable to recover from myocardial cell loss due to cardiac ischemia and infarction because terminally differentiated cardiomyocytes proliferate at a low rate. However, cardiomyocytes in other vertebrate animal models such as zebrafish, axolotls, newts and mammalian mouse neonates are capable of de-differentiating in order to promote cardiomyocyte proliferation and subsequent cardiac regeneration after injury. Although de-differentiation may occur in adult mammalian cardiomyocytes, it is typically associated with diseased hearts and pathologic remodeling rather than repair and regeneration. Here, we review recent studies of cardiac development, regeneration and disease that highlight how changes in myocardial identity (plasticity) is regulated and impacts adaptive and maladaptive cardiac responses.
成年哺乳动物的心脏无法从因心脏缺血和梗死导致的心肌细胞损失中恢复，因为终末分化的心肌细胞增殖速率很低。然而，在其他脊椎动物模型（如斑马鱼、蝾螈、娃娃鱼）以及新生哺乳动物小鼠中，心肌细胞能够去分化，以促进心肌细胞增殖以及损伤后的心脏再生。尽管成年哺乳动物心肌细胞可能会发生去分化，但这通常与患病心脏及病理重塑相关，而非修复和再生。在此，我们综述了近期关于心脏发育、再生和疾病的研究，这些研究突出了心肌特性（可塑性）的变化是如何被调控的，以及如何影响适应性和适应不良性心脏反应。
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