De Felice Mario, Di Lauro Roberto
Stazione Zoologica Anton Dohrn, University of Naples Federico II, 80121 Naples, Italy.
Endocr Rev. 2004 Oct;25(5):722-46. doi: 10.1210/er.2003-0028.
Thyroid gland organogenesis results in an organ the shape, size, and position of which are largely conserved among adult individuals of the same species, thus suggesting that genetic factors must be involved in controlling these parameters. In humans, the organogenesis of the thyroid gland is often disturbed, leading to a variety of conditions, such as agenesis, ectopy, and hypoplasia, which are collectively called thyroid dysgenesis (TD). The molecular mechanisms leading to TD are largely unknown. Studies in murine models and in a few patients with dysgenesis revealed that mutations in regulatory genes expressed in the developing thyroid are responsible for this condition, thus showing that TD can be a genetic and inheritable disease. These studies open the way to a novel working hypothesis on the molecular and genetic basis of this frequent human condition and render the thyroid an important model in the understanding of molecular mechanisms regulating the size, shape, and position of organs.
甲状腺器官发生形成的器官,其形状、大小和位置在同一物种的成年个体中基本保持一致,这表明遗传因素必定参与了对这些参数的控制。在人类中,甲状腺器官发生常常受到干扰,导致多种病症,如甲状腺缺如、异位和发育不全,这些病症统称为甲状腺发育异常(TD)。导致TD的分子机制在很大程度上尚不清楚。对小鼠模型和少数发育异常患者的研究表明,在发育中的甲状腺中表达的调控基因突变是导致这种病症的原因,这表明TD可能是一种遗传性疾病。这些研究为关于这种常见人类病症的分子和遗传基础的新工作假设开辟了道路,并使甲状腺成为理解调节器官大小、形状和位置的分子机制的重要模型。