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首页> 外文期刊>Studies in Health Technology and Informatics >Etiologic Theories of Idiopathic Scoliosis: The Breaking of Bilateral Symmetry in Relation to Left-Right Asymmetry of Internal Organs, Right Thoracic Adolescent Idiopathic Scoliosis (AIS) and Vertebrate Evolution
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Etiologic Theories of Idiopathic Scoliosis: The Breaking of Bilateral Symmetry in Relation to Left-Right Asymmetry of Internal Organs, Right Thoracic Adolescent Idiopathic Scoliosis (AIS) and Vertebrate Evolution

机译：特发性脊柱侧凸的病因学理论：双边对称性与内脏左右不对称性，右胸青春期特发性脊柱侧弯（AIS）和脊椎动物进化有关的打破

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摘要

In the search to understand the etiology and pathogenesis of adolescent idiopathic scoliosis (AIS) some workers have focused on mechanisms initiated in embryonic life including a disturbance of bilateral (left-right or mirror-image) symmetry highly conserved in vertebrates. The normal external bilateral symmetry of vertebrates results from a default process involving mesodermal somites. The normal internal asymmetry of the heart, major blood vessels, lungs and gut with its glands is also highly conserved among vertebrates. It results from the breaking of the initial bilateral symmetry by a binary asymmetry switch mechanism producing asymmetric gene expression around the embryonic node and/or in the lateral plate mesoderm. In the mouse this switch occurs during gastrulation by cilia driving a leftward flow of fluid and morphogen(s) at the embryonic node (nodal flow) that favors precursors of the heart, great vessels and viscera on the left. Based on the non-random laterality of thoracic AIS curves, the hypothesis is suggested that an anomaly of the binary asymmetry switch explains the excess of right/left thoracic AIS. Some support for this hypothesis is the prevalence of right and left scoliosis curve laterality associated with situs inversus. There is recent evidence that vertebrates within their bilateralised shell retain an archaic left-right asymmetric visceral body organization evident in thoracic and abdominal organs.
机译：为了了解青少年特发性脊柱侧凸（AIS）的病因和发病机理，一些工作人员集中在胚胎生命中引发的机制上，包括在脊椎动物中高度保守的双边（左右或对称）对称性紊乱。脊椎动物的正常外部双侧对称性来自涉及中胚层体的默认过程。在脊椎动物中，心脏，主要血管，肺和肠道及其腺体的正常内部不对称性也高度保守。这是由于通过二进制不对称转换机制破坏了初始的双边对称性而产生的，该机制在胚胎结点周围和/或外侧板中胚层中产生了不对称的基因表达。在小鼠中，此开关在纤毛形成过程中通过纤毛在胚胎结点处驱动流体和形态发生剂向左流动（淋巴流）而发生，有利于心脏，大血管和内脏的前体。基于胸部AIS曲线的非随机性，提出了这样的假设：二元不对称开关的异常解释了右/左胸AIS的过多。这种假设的一些支持是与位姿倒置相关的左右脊柱侧弯曲线偏侧的普遍性。最近有证据表明，脊椎动物在其双侧壳内保留着一种古老的左右不对称内脏身体组织，在胸腔和腹部器官中都很明显。

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