Gibson Beth G, Briggs Michael D
Institute of Genetic Medicine, Newcastle University, Newcastle-upon-Tyne, NE1 3BZ, UK.
International Centre for Life, Central Parkway, Newcastle upon Tyne, NE1 3BZ, UK.
Orphanet J Rare Dis. 2016 Jun 28;11(1):86. doi: 10.1186/s13023-016-0459-2.
The large chondroitin sulphated proteoglycan aggrecan (ACAN) is the most abundant non-collagenous protein in cartilage and is essential for its structure and function. Mutations in ACAN result in a broad phenotypic spectrum of non-lethal skeletal dysplasias including spondyloepimetaphyseal dysplasia, spondyloepiphyseal dysplasia, familial osteochondritis dissecans and various undefined short stature syndromes associated with accelerated bone maturation. However, very little is currently known about the disease pathways that underlie these aggrecanopathies, although they are likely to be a combination of haploinsufficiency and dominant-negative (neomorphic) mechanisms. This review discusses the known human and animal aggrecanopathies in the context of clinical presentation and potential disease mechanisms.
大型硫酸软骨素蛋白聚糖聚集蛋白聚糖(ACAN)是软骨中最丰富的非胶原蛋白,对其结构和功能至关重要。ACAN基因突变会导致一系列非致死性骨骼发育不良的广泛表型谱,包括脊椎骨骺发育异常、脊椎骨骺发育不良、家族性剥脱性骨软骨炎以及各种与骨成熟加速相关的不明原因的身材矮小综合征。然而,目前对于这些聚集蛋白聚糖病的发病机制知之甚少,尽管它们可能是单倍剂量不足和显性负性(新形态)机制的组合。本综述在临床表现和潜在疾病机制的背景下讨论了已知的人类和动物聚集蛋白聚糖病。