当前位置: X-MOL 学术Circ. Res. › 论文详情
Our official English website, www.x-mol.net, welcomes your feedback! (Note: you will need to create a separate account there.)
Polyploidy in Cardiomyocytes: Roadblock to Heart Regeneration?
Circulation Research ( IF 16.5 ) Pub Date : 2020-02-13 , DOI: 10.1161/circresaha.119.315408
Wouter Derks 1 , Olaf Bergmann 1, 2
Affiliation  

The hallmark of most cardiac diseases is the progressive loss of cardiomyocytes. In the perinatal period, cardiomyocytes still proliferate, and the heart shows the capacity to regenerate upon injury. In the adult heart, however, the actual rate of cardiomyocyte renewal is too low to efficiently counteract substantial cell loss caused by cardiac injury. In mammals, cardiac growth by cell number expansion changes to growth by cardiomyocyte enlargement soon after birth, coinciding with a period in which most cardiomyocytes increase their DNA content by multinucleation and nuclear polyploidization. Although cardiomyocyte hypertrophy is often associated with these processes, whether polyploidy is a prerequisite or a consequence of hypertrophic growth is unclear. Both the benefits of cardiomyocyte enlargement over proliferative growth of the heart and the physiological role of polyploidy in cardiomyocytes are enigmatic. Interestingly, hearts in animal species with substantial cardiac regenerative capacity dominantly comprise diploid cardiomyocytes, raising the hypothesis that cardiomyocyte polyploidy poses a barrier for cardiomyocyte proliferation and subsequent heart regeneration. On the contrary, there is also evidence for self-duplication of multinucleated myocytes, suggesting a more complex picture of polyploidy in heart regeneration. Polyploidy is not restricted to the heart but also occurs in other cell types in the body. In this review, we explore the biological relevance of polyploidy in different species and tissues to acquire insight into its specific role in cardiomyocytes. Furthermore, we speculate about the physiological role of polyploidy in cardiomyocytes and how this might relate to renewal and regeneration.

中文翻译:

心肌细胞中的多倍性:心脏再生的障碍吗?

大多数心脏疾病的标志是心肌细胞的逐渐丧失。在围产期,心肌细胞仍在增殖,心脏显示出在受伤时能够再生的能力。然而,在成年心脏中,心肌细胞的实际更新速率太低,无法有效抵消由心脏损伤引起的实质性细胞丢失。在哺乳动物中,出生后不久,通过细胞数量膨胀引起的心脏生长变为通过心肌细胞增大引起的生长,这与大多数心肌细胞通过多核化和核多倍化增加其DNA含量的时期相吻合。尽管心肌细胞肥大通常与这些过程有关,但不清楚多倍体是肥大生长的前提还是后果。心肌细胞对心脏增生生长的好处以及多倍体在心肌细胞中的生理作用都难以言喻。有趣的是,具有实质心脏再生能力的动物物种的心脏主要包含二倍体心肌细胞,从而提出了心肌细胞多倍体构成心肌细胞增殖和随后的心脏再生障碍的假设。相反,也有证据表明多核肌细胞会自我复制,这提示心脏再生过程中多倍体的情况更为复杂。多倍体不仅限于心脏,还可以在体内其他细胞类型中发生。在这篇综述中,我们探讨了多倍体在不同物种和组织中的生物学相关性,以了解其在心肌细胞中的特定作用。此外,
更新日期:2020-02-14
down
wechat
bug