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Notch 及其相互作用的信号通路在心脏发育、疾病和再生中的作用。

Notch and interacting signalling pathways in cardiac development, disease, and regeneration.

机构信息

Intercellular Signalling in Cardiovascular Development and Disease Laboratory, Centro Nacional de Investigaciones Cardiovasculares Carlos III (CNIC), Madrid, Spain.

CIBER CV, Instituto de Salud Carlos III, Madrid, Spain.

出版信息

Nat Rev Cardiol. 2018 Nov;15(11):685-704. doi: 10.1038/s41569-018-0100-2.

DOI:10.1038/s41569-018-0100-2
PMID:30287945
Abstract

Cardiogenesis is a complex developmental process involving multiple overlapping stages of cell fate specification, proliferation, differentiation, and morphogenesis. Precise spatiotemporal coordination between the different cardiogenic processes is ensured by intercellular signalling crosstalk and tissue-tissue interactions. Notch is an intercellular signalling pathway crucial for cell fate decisions during multicellular organismal development and is aptly positioned to coordinate the complex signalling crosstalk required for progressive cell lineage restriction during cardiogenesis. In this Review, we describe the role of Notch signalling and the crosstalk with other signalling pathways during the differentiation and patterning of the different cardiac tissues and in cardiac valve and ventricular chamber development. We examine how perturbation of Notch signalling activity is linked to congenital heart diseases affecting the neonate and adult, and discuss studies that shed light on the role of Notch signalling in heart regeneration and repair after injury.

摘要

心脏发生是一个复杂的发育过程,涉及多个重叠的细胞命运特化、增殖、分化和形态发生阶段。不同心脏发生过程之间的精确时空协调是通过细胞间信号转导的串扰和组织-组织相互作用来保证的。Notch 是细胞间信号通路,在多细胞生物体的发育过程中对于细胞命运决定至关重要,并且处于适当的位置,以协调在心脏发生过程中进行渐进性细胞谱系限制所需的复杂信号转导串扰。在这篇综述中,我们描述了 Notch 信号在不同心脏组织的分化和模式形成以及心脏瓣膜和心室腔发育中的作用,以及 Notch 信号与其他信号通路的串扰。我们研究了 Notch 信号活性的扰动如何与影响新生儿和成人的先天性心脏病相关,并讨论了阐明 Notch 信号在损伤后心脏再生和修复中的作用的研究。

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Notch and interacting signalling pathways in cardiac development, disease, and regeneration.Notch 及其相互作用的信号通路在心脏发育、疾病和再生中的作用。
Nat Rev Cardiol. 2018 Nov;15(11):685-704. doi: 10.1038/s41569-018-0100-2.
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