Esophagus and trachea arise from a common origin, the anterior foregut tube. The compartmentalization process of the foregut into the esophagus and trachea is still poorly understood. Esophageal atresia/tracheoesophageal fistula (EA/TEF) is one of the most common gastrointestinal congenital defects with an incidence rate of 1 in 2,500 births. EA/TEF is linked to the disruption of the compartmentalization process of the foregut tube. In EA/TEF patients, other organ anomalies and disorders have also been reported. Over the last two decades, animal models have shown the involvement of multiple signaling pathways and transcription factors in the development of the esophagus and trachea. Use of induced pluripotent stem cells (iPSCs) to understand organogenesis has been a valuable tool for mimicking gastrointestinal and respiratory organs. This review focuses on the signaling mechanisms involved in esophageal development and the use of iPSCs to model and understand it.

中文翻译：

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用于研究气管-食管分离和食管发育的遗传小鼠模型和诱导多能干细胞。

食道和气管起源于一个共同的起源，即前前肠管。前肠进入食道和气管的分隔过程仍然知之甚少。食管闭锁/气管食管瘘 (EA/TEF) 是最常见的胃肠道先天性缺陷之一，发病率为每 2,500 个新生儿中就有 1 个。EA/TEF 与前肠管区室化过程的中断有关。在 EA/TEF 患者中，还报道了其他器官异常和病症。在过去的二十年里，动物模型表明多种信号通路和转录因子参与了食道和气管的发育。使用诱导多能干细胞 (iPSC) 了解器官发生是模拟胃肠道和呼吸器官的宝贵工具。