Cardiac developmental disorders represent the most common of human birth defects, and anomalies in cardiomyocyte proliferation drive many of these disorders. This review highlights the molecular mechanisms of prenatal cardiac growth. Trabeculation represents the initial ventricular growth phase and is necessary for embryonic survival. Later in development, the bulk of the ventricular wall derives from the compaction process, yet the arrest of this process can still be compatible with life. Cardiomyocyte proliferation and growth form the basis of both trabeculation and compaction, and mouse models indicate that cardiomyocyte interactions with the surrounding environment are critical for these proliferative processes. The human genetics of left ventricular noncompaction cardiomyopathy suggest that cardiomyocyte cell-autonomous mechanisms contribute to the compaction process. Understanding the determinants of prenatal or early postnatal cardiomyocyte proliferation and growth provides critical information that identifies risk factors for cardiovascular disease, including heart failure and its associated complications of arrhythmias and thromboembolic events.

中文翻译：

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心脏发育障碍的遗传学：心肌细胞增殖和生长以及与心力衰竭的相关性。

心脏发育障碍代表了最常见的人类出生缺陷，心肌细胞增殖异常导致了许多此类疾病。这篇综述强调了产前心脏生长的分子机制。小梁代表初始心室生长期并且是胚胎存活所必需的。在后来的发展中，大部分心室壁来自压实过程，但这个过程的停止仍然可以与生命相容。心肌细胞增殖和生长形成小梁形成和压实的基础，小鼠模型表明心肌细胞与周围环境的相互作用对于这些增殖过程至关重要。左心室致密化不全心肌病的人类遗传学表明，心肌细胞自主机制有助于致密化过程。了解产前或产后早期心肌细胞增殖和生长的决定因素提供了确定心血管疾病危险因素的关键信息，包括心力衰竭及其相关的心律失常并发症和血栓栓塞事件。