Academic Endocrine Unit, Nuffield Department of Clinical Medicine, Oxford Centre for Diabetes, Endocrinology, and Metabolism, Churchill Hospital, University of Oxford, Headington, Oxford, United Kingdom.
Ann N Y Acad Sci. 2011 Nov;1237:24-38. doi: 10.1111/j.1749-6632.2011.06221.x.
Parathyroid developmental anomalies, which result in hypoparathyroidism, are common and may occur in one in 4,000 live births. Parathyroids, in man, develop from the endodermal cells of the third and fourth pharyngeal pouches, whereas, in the mouse they develop solely from the endoderm of the third pharyngeal pouches. In addition, neural crest cells that arise from the embryonic mid- and hindbrain also contribute to parathyroid gland development. The molecular signaling pathways that are involved in determining the differentiation of the pharyngeal pouch endoderm into parathyroid cells are being elucidated by studies of patients with hypoparathyroidism and appropriate mouse models. These studies have revealed important roles for a number of transcription factors, which include Tbx1, Gata3, Gcm2, Sox3, Aire1 and members of the homeobox (Hox) and paired box (Pax) families.
甲状旁腺发育异常导致甲状旁腺功能减退症较为常见，其在活产婴儿中的发病率约为 1/4000。人类的甲状旁腺起源于第三和第四咽囊的内胚层细胞，而在小鼠中，它们仅由第三咽囊的内胚层发育而来。此外，从中胚层和后脑起源的神经嵴细胞也有助于甲状旁腺的发育。通过对甲状旁腺功能减退症患者和适当的小鼠模型的研究，正在阐明参与确定咽囊内胚层分化为甲状旁腺细胞的分子信号通路。这些研究揭示了许多转录因子的重要作用，包括 Tbx1、Gata3、Gcm2、Sox3、Aire1 以及同源盒（Hox）和配对盒（Pax）家族的成员。
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