Cardiomyocyte Proliferation from Fetal- to Adult- and from Normal- to Hypertrophy and Failing Hearts.
Cardiomyocyte Proliferation from Fetal- to Adult- and from Normal- to Hypertrophy and Failing Hearts.
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DOI：
10.3390/biology11060880
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发表时间：
2022-06-08
期刊：
影响因子：
4.2
通讯作者：
Ye, Lei
中科院分区：
文献类型：
--
作者：
Bishop, Sanford P.;Zhang, Jianyi;Ye, Lei
各种原因造成的心脏损伤死亡仍然是全世界死亡的主要原因。心肌细胞是心脏的主要收缩细胞，负责将血液泵送到身体的其他部位。在胎儿发育过程中，这些未成熟的心肌细胞很小，当它们发展出阻止进一步分裂的成熟细胞的结构和功能特征时，它们迅速分裂以完成出生时的心脏发育。出生后心脏的所有进一步生长都是由于心肌细胞的大小增加，即肥大。由于冠状动脉阻塞或其他原因导致功能性心肌细胞丧失后，心脏无法取代失去的细胞。诱导成年心肌细胞重新激活细胞周期和修复心脏损伤一直是重要的研究目标之一。这篇综述探讨了发育，结构和功能的变化，不断增长的心肌细胞，特别是肌节，负责力的产生，从早期胎儿期的生殖细胞生长通过新生儿期和成年期，以及在病理反应不同形式的心肌疾病或损伤。在正常或患病条件下，心肌细胞细胞周期调控相关的多个问题进行了讨论。心肌细胞从早期胎儿阶段的增生性细胞生长，通过出生和转化为肥大细胞生长，持续到成人阶段并对心肌上的各种形式的应激作出反应，在结构、代谢和功能上经历急剧变化，通常导致心肌衰竭。具有不完全形成的肌节和其他细胞和细胞外成分的胎儿细胞正在积极地进行有丝分裂、细胞器分散和子细胞的形成。在新生儿生命的最初几天，心脏能够从损伤中完全修复，但不能在转化为肥大生长后修复。结构和代谢变化发生后转化为肥大生长，形成进一步心肌细胞分裂的障碍，虽然间质成分继续分裂，以跟上心脏生长的步伐。应激心肌发生细胞内外结构改变，与血流动力学改变一起导致心肌衰竭的代谢和功能改变。这篇评论探讨了一些问题，有关条件，调节正常和病理性生长的心脏。
Death from injury to the heart from a variety of causes remains a major cause of mortality worldwide. The cardiomyocyte, the major contracting cell of the heart, is responsible for pumping blood to the rest of the body. During fetal development, these immature cardiomyocytes are small and rapidly divide to complete development of the heart by birth when they develop structural and functional characteristics of mature cells which prevent further division. All further growth of the heart after birth is due to an increase in the size of cardiomyocytes, hypertrophy. Following the loss of functional cardiomyocytes due to coronary artery occlusion or other causes, the heart is unable to replace the lost cells. One of the significant research goals has been to induce adult cardiomyocytes to reactivate the cell cycle and repair cardiac injury. This review explores the developmental, structural, and functional changes of the growing cardiomyocyte, and particularly the sarcomere, responsible for force generation, from the early fetal period of reproductive cell growth through the neonatal period and on to adulthood, as well as during pathological response to different forms of myocardial diseases or injury. Multiple issues relative to cardiomyocyte cell-cycle regulation in normal or diseased conditions are discussed. The cardiomyocyte undergoes dramatic changes in structure, metabolism, and function from the early fetal stage of hyperplastic cell growth, through birth and the conversion to hypertrophic cell growth, continuing to the adult stage and responding to various forms of stress on the myocardium, often leading to myocardial failure. The fetal cell with incompletely formed sarcomeres and other cellular and extracellular components is actively undergoing mitosis, organelle dispersion, and formation of daughter cells. In the first few days of neonatal life, the heart is able to repair fully from injury, but not after conversion to hypertrophic growth. Structural and metabolic changes occur following conversion to hypertrophic growth which forms a barrier to further cardiomyocyte division, though interstitial components continue dividing to keep pace with cardiac growth. Both intra- and extracellular structural changes occur in the stressed myocardium which together with hemodynamic alterations lead to metabolic and functional alterations of myocardial failure. This review probes some of the questions regarding conditions that regulate normal and pathologic growth of the heart.
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影响因子：
5
作者：
Arai, M;Suzuki, T;Nagai, R
通讯作者：
Nagai, R
影响因子：
10.8
作者：
Bache, RJ;Zhang, JY;Ugurbil, K
通讯作者：
Ugurbil, K
影响因子：
15.9
作者：
Asai, K;Yang, GP;Vatner, SF
通讯作者：
Vatner, SF
DOI：
10.1249/00005768-198606000-00009
发表时间：
1986-06-01
期刊：
MEDICINE AND SCIENCE IN SPORTS AND EXERCISE
影响因子：
--
作者：
ALPERT, NR;MULIERI, LA
通讯作者：
MULIERI, LA
影响因子：
20.1
作者：
ANVERSA, P;LEVICKY, V;KIKKAWA, Y
通讯作者：
KIKKAWA, Y