Molecular and cellular basis of embryonic cardiac chamber maturation.

Molecular and cellular basis of embryonic cardiac chamber maturation.
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胚胎心脏腔室成熟的分子和细胞基础。

DOI:
10.1016/j.semcdb.2021.04.022
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发表时间:
2021-10
影响因子:
7.3
通讯作者:
Liu J
Liu J
中科院分区:
生物学2区
文献类型:
--
作者:
Dong Y;Qian L;Liu J

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心脏畸形是导致人类出生缺陷的主要原因,许多先天性心脏病(CHD)起源于影响心脏发育和成熟的遗传缺陷。在发育过程中,脊椎动物的心脏经历了一系列复杂的形态发生过程,增加了泵血的能力。其中一个过程导致形成手指状的肌肉突起,称为小梁。小梁增加心输出量,并在冠状动脉血管化之前允许胚胎心肌吸收营养和氧气,而不会增加心脏大小。心脏小梁形成对于心室内快速传导系统的发育也是至关重要的。心脏小梁发育的改变可以表现为各种先天性缺陷,如左心室致密化不全。本文就近年来有关心脏小梁发育的分子和细胞机制的研究进展作一综述。
Heart malformation is the leading cause of human birth defects, and many of the congenital heart diseases (CHDs) originate from genetic defects that impact cardiac development and maturation. During development, the vertebrate heart undergoes a series of complex morphogenetic processes that increase its ability to pump blood. One of these processes leads to the formation of the finger-like muscular projections called trabeculae. Trabeculae increase cardiac output and permit nutrition and oxygen uptake in the embryonic myocardium prior to coronary vascularization without increasing heart size. Cardiac trabeculation is also crucial for the development of the intraventricular fast conduction system. Alterations in cardiac trabecular development can manifest as a variety of congenital defects such as left ventricular noncompaction. In this review, we discuss the latest advances in understanding the molecular and cellular mechanisms underlying cardiac trabecular development.
DOI: 10.1203/00006450-199905010-00004
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