软骨发育不全
骨形态发生蛋白
骨化
骨关节炎
后纵韧带
医学
成纤维细胞生长因子受体
成纤维细胞生长因子
阿达姆斯
Wnt信号通路
椎管狭窄
椎管
软骨
成纤维细胞生长因子受体3
SMAD公司
遗传学
椎管狭窄
病理
解剖
基因
生物
脊髓
受体
神经科学
基质金属蛋白酶
金属蛋白酶
血栓反应素
替代医学
腰椎
作者
Vadim A. Byvaltsev,А. А. Калинин,Phillip A. Hernandez,Valerii V Shepelev,Yu.Ya. Pestryakov,Marat A. Aliyev,Morgan B. Giers
标识
DOI:10.3390/ijms232113479
摘要
Spinal stenosis (SS) is a multifactorial polyetiological condition characterized by the narrowing of the spinal canal. This condition is a common source of pain among people over 50 years old. We perform a systematic review of molecular and genetic mechanisms that cause SS. The five main mechanisms of SS were found to be ossification of the posterior longitudinal ligament (OPLL), hypertrophy and ossification of the ligamentum flavum (HLF/OLF), facet joint (FJ) osteoarthritis, herniation of the intervertebral disc (IVD), and achondroplasia. FJ osteoarthritis, OPLL, and HLF/OLFLF/OLF have all been associated with an over-abundance of transforming growth factor beta and genes related to this phenomenon. OPLL has also been associated with increased bone morphogenetic protein 2. FJ osteoarthritis is additionally associated with Wnt/β-catenin signaling and genes. IVD herniation is associated with collagen type I alpha 1 and 2 gene mutations and subsequent protein dysregulation. Finally, achondroplasia is associated with fibroblast growth factor receptor 3 gene mutations and fibroblast growth factor signaling. Although most publications lack data on a direct relationship between the mutation and SS formation, it is clear that genetics has a direct impact on the formation of any pathology, including SS. Further studies are necessary to understand the genetic and molecular changes associated with SS.
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