The vertebrate heart tube forms from epithelial progenitor cells in the early embryo and subsequently elongates by progressive addition of second heart field (SHF) progenitor cells from adjacent splanchnic mesoderm. Failure to maximally elongate the heart results in a spectrum of morphological defects affecting the cardiac poles, including outflow tract alignment and atrioventricular septal defects, among the most common congenital birth anomalies. SHF cells constitute an atypical apicobasally polarized epithelium with dynamic basal filopodia, located in the dorsal wall of the pericardial cavity. Recent studies have highlighted the importance of epithelial architecture and cell adhesion in the SHF, particularly for signaling events that control the progenitor cell niche during heart tube elongation. The 22q11.2 deletion syndrome gene Tbx1 regulates progenitor cell status through modulating cell shape and filopodial activity and is required for SHF contributions to both cardiac poles. Noncanonical Wnt signaling and planar cell polarity pathway genes control epithelial polarity in the dorsal pericardial wall, as progenitor cells differentiate in a transition zone at the arterial pole. Defects in these pathways lead to outflow tract shortening. Moreover, new biomechanical models of heart tube elongation have been proposed based on analysis of tissue-wide forces driving epithelial morphogenesis in the SHF, including regional cell intercalation, cell cohesion, and epithelial tension. Regulation of the epithelial properties of SHF cells is thus emerging as a key step during heart tube elongation, adding a new facet to our understanding of the mechanisms underlying both heart morphogenesis and congenital heart defects.

脊椎动物心管由早期胚胎中的上皮祖细胞形成，并随后通过逐渐添加来自相邻内脏中胚层的第二心脏场（SHF）祖细胞而伸长。无法最大程度地延长心脏的活动会导致一系列影响心脏两极的形态学缺陷，包括流出道对齐和房室间隔缺损，这是最常见的先天性出生异常。SHF细胞位于心包腔的背壁，构成具有动态基底丝状伪足的非典型的oba突上皮极化的上皮。最近的研究突出了SHF中上皮结构和细胞粘附的重要性，特别是对于在心管延长过程中控制祖细胞生态位的信号传递事件。22q11.2缺失综合征基因Tbx1通过调节细胞形状和丝虫活动来调节祖细胞状态，这是SHF对两个心脏极的贡献所必需的。由于祖细胞在动脉极的过渡区分化，非经典的Wnt信号传导和平面细胞极性通路基因控制着心包后壁的上皮极性。这些途径的缺陷导致流出道缩短。此外，已经基于对驱动SHF中上皮形态发生的组织范围的力的分析的基础上，提出了新的心管伸长的生物力学模型，包括区域细胞插层，细胞内聚力和上皮张力。因此，对SHF细胞上皮特性的调节已成为心导管延长过程中的关键步骤，