Department of Pathology, Institute of Biomedicine, The Sahlgrenska Academy at the University of Gothenburg, Gula Stråket 8, 413 45 Göteborg, Sweden.
J Mol Endocrinol. 2011 Feb;46(1):R33-42. doi: 10.1677/jme-10-0084.
The thyroid develops from the foregut endoderm. Yet uncharacterized inductive signals specify endoderm progenitors to a thyroid cell fate that assembles in the pharyngeal floor from which the primordium buds and migrates to the final position of the gland. The morphogenetic process is regulated by both cell-autonomous (e.g. activated by NKX2-1, FOXE1, PAX8, and HHEX) and mesoderm-derived (e.g. mediated by TBX1 and fibroblast growth factors) mechanisms acting in concert to promote growth and survival of progenitor cells. The developmental role of TSH is limited to thyroid differentiation set to work after the gross anatomy of the gland is already sculptured. This review summarizes recent advances on the molecular genetics of thyroid morphogenesis put into context of endoderm developmental traits and highlights established and novel mechanisms of thyroid dysgenesis of potential relevance to congenital hypothyroidism in man.
甲状腺由前肠内胚层发育而来。然而，尚未确定的诱导信号将内胚层祖细胞特化为甲状腺细胞命运，这些细胞在前咽底部分化形成原基，并迁移到腺体的最终位置。形态发生过程受细胞自主（例如，由 NKX2-1、FOXE1、PAX8 和 HHEX 激活）和中胚层衍生（例如，由 TBX1 和成纤维细胞生长因子介导）机制的调节，这些机制协同作用促进祖细胞的生长和存活。TSH 的发育作用仅限于在腺体的大体解剖结构已经塑造后开始作用的甲状腺分化。本综述总结了甲状腺形态发生的分子遗传学的最新进展，将其置于内胚层发育特征的背景下，并强调了甲状腺发育不良的已建立和新机制，这些机制可能与人类先天性甲状腺功能减退症有关。
