Department of Pathology and Laboratory Medicine, University of North Carolina, Chapel Hill, NC 27599, USA; McAllister Heart Institute, University of North Carolina, Chapel Hill, NC 27599, USA.
Department of Pathology and Laboratory Medicine, University of North Carolina, Chapel Hill, NC 27599, USA; McAllister Heart Institute, University of North Carolina, Chapel Hill, NC 27599, USA.
Semin Cell Dev Biol. 2021 Oct;118:144-149. doi: 10.1016/j.semcdb.2021.04.022. Epub 2021 May 11.
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 sheet-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.
心脏畸形是人类出生缺陷的主要原因,许多先天性心脏病(CHD)源于影响心脏发育和成熟的遗传缺陷。在发育过程中,脊椎动物心脏经历了一系列复杂的形态发生过程,从而提高了其泵血能力。其中一个过程导致了板状肌肉突起的形成,这些突起被称为小梁。小梁增加了心输出量,并允许胚胎心肌在冠状动脉血管化之前摄取营养和氧气,而不会增加心脏大小。心脏小梁化对于心室内快速传导系统的发育也至关重要。心脏小梁发育的改变可能表现为各种先天性缺陷,如左心室肥厚。在这篇综述中,我们讨论了理解心脏小梁发育背后的分子和细胞机制的最新进展。