OI is a genetically diverse disorder characterized by bone fragility and deformities, with most cases attributed to dominant mutations in collagen I-related genes. However, mutations in TENT5A, encoding a poly(A) polymerase, have recently been implicated in severe, recessive forms of OI. We reported 3 individuals from a consanguineous family with a novel homozygous TENT5A variant (c.672G>T, p.Arg224Ser). Our patients presented with severe bone fragility, generalized osteopenia, skeletal deformities, short stature, and early wheelchair dependence. Patient-derived fibroblasts demonstrated impaired collagen secretion and disorganized fibril network formation. Our findings provide new insights into the complex pathophysiology of TENT5A-associated OI and underscore the need for further research into its role in skeletal homeostasis.
TENT5A-associated osteogenesis imperfecta: long-term follow-up and molecular insights.
TENT5A 相关性成骨不全:长期随访和分子见解
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作者:Stasek Stefanie, Zaucke Frank, Stephan Alice, Etich Julia, Mörgelin Matthias, Baumann Ulrich, Rehberg Mirko, Reincke Susanna, Semler Oliver, Hoyer-Kuhn Heike
| 期刊: | JBMR Plus | 影响因子: | 2.400 |
| 时间: | 2025 | 起止号: | 2025 May 11; 9(7):ziaf083 |
| doi: | 10.1093/jbmrpl/ziaf083 | 研究方向: | 骨科研究 |
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