• 文献检索
  • 文档翻译
  • 深度研究
  • 学术资讯
  • Suppr Zotero 插件Zotero 插件
  • 邀请有礼
  • 套餐&价格
  • 历史记录
应用&插件
Suppr Zotero 插件Zotero 插件浏览器插件Mac 客户端Windows 客户端微信小程序
定价
高级版会员购买积分包购买API积分包
服务
文献检索文档翻译深度研究API 文档MCP 服务
关于我们
关于 Suppr公司介绍联系我们用户协议隐私条款
关注我们

Suppr 超能文献

核心技术专利:CN118964589B侵权必究
粤ICP备2023148730 号-1Suppr @ 2026

文献检索

告别复杂PubMed语法,用中文像聊天一样搜索,搜遍4000万医学文献。AI智能推荐,让科研检索更轻松。

立即免费搜索

文件翻译

保留排版,准确专业,支持PDF/Word/PPT等文件格式,支持 12+语言互译。

免费翻译文档

深度研究

AI帮你快速写综述,25分钟生成高质量综述,智能提取关键信息,辅助科研写作。

立即免费体验

轻度肌病与 COMP 相关,但与遗传骨骼疾病的小鼠模型中的 MATN3 突变无关。

Mild myopathy is associated with COMP but not MATN3 mutations in mouse models of genetic skeletal diseases.

机构信息

Institute of Genetic Medicine, Newcastle University, Newcastle upon Tyne, United Kingdom.

出版信息

PLoS One. 2013 Nov 27;8(11):e82412. doi: 10.1371/journal.pone.0082412. eCollection 2013.

DOI:10.1371/journal.pone.0082412
PMID:24312420
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3842254/
Abstract

Pseudoachondroplasia (PSACH) and multiple epiphyseal dysplasia (MED) are skeletal disorders resulting from mutations in COMP, matrilin-3 or collagen IX and are characterised by short-limbed dwarfism and premature osteoarthritis. Interestingly, recent reports suggest patients can also manifest with muscle weakness. Here we present a detailed analysis of two mouse models of the PSACH/MED disease spectrum; ΔD469 T3-COMP (PSACH) and V194D matrilin-3 (MED). In grip test experiments T3-COMP mice were weaker than wild-type littermates, whereas V194D mice behaved as controls, confirming that short-limbed dwarfism alone does not contribute to PSACH/MED-related muscle weakness. Muscles from T3-COMP mice showed an increase in centronuclear fibers at the myotendinous junction. T3-COMP tendons became more lax in cyclic testing and showed thicker collagen fibers when compared with wild-type tissue; matrilin-3 mutant tissues were indistinguishable from controls. This comprehensive study of the myopathy associated with PSACH/MED mutations enables a better understanding of the disease progression, confirms that it is genotype specific and that the limb weakness originates from muscle and tendon pathology rather than short-limbed dwarfism itself. Since some patients are primarily diagnosed with neuromuscular symptoms, this study will facilitate better awareness of the differential diagnoses that might be associated with the PSACH/MED spectrum and subsequent care of PSACH/MED patients.

摘要

假性软骨发育不全症(PSACH)和多发性骨骺发育不良症(MED)是由 COMP、软骨寡聚基质蛋白-3 或胶原 IX 基因突变引起的骨骼疾病,其特征为短肢侏儒症和骨关节炎。有趣的是,最近的报告表明,患者也可能表现出肌肉无力。在这里,我们对 PSACH/MED 疾病谱的两种小鼠模型进行了详细分析;ΔD469 T3-COMP(PSACH)和 V194D 软骨寡聚基质蛋白-3(MED)。在握力测试实验中,T3-COMP 小鼠比野生型同窝仔鼠弱,而 V194D 小鼠的行为与对照鼠相同,这证实了单纯的短肢侏儒症并不导致 PSACH/MED 相关的肌肉无力。T3-COMP 小鼠的肌肉在肌肌腱交界处出现中心核纤维增加。与野生型组织相比,T3-COMP 肌腱在循环测试中变得更加松弛,并且胶原纤维更厚;软骨寡聚基质蛋白-3 突变组织与对照组织没有区别。这项对与 PSACH/MED 突变相关的肌病的综合研究使我们能够更好地理解疾病进展,证实它是特定于基因型的,并且肢体无力源自肌肉和肌腱病理,而不是短肢侏儒症本身。由于一些患者主要被诊断为神经肌肉症状,因此这项研究将有助于更好地了解可能与 PSACH/MED 谱相关的鉴别诊断,并为 PSACH/MED 患者提供后续护理。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/367b/3842254/a5d2f25db137/pone.0082412.g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/367b/3842254/e63f410d0cc4/pone.0082412.g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/367b/3842254/652e589cba3f/pone.0082412.g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/367b/3842254/3e6762f4b4f8/pone.0082412.g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/367b/3842254/e6cf954df91a/pone.0082412.g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/367b/3842254/a424d7516b67/pone.0082412.g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/367b/3842254/40c5907fcfa6/pone.0082412.g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/367b/3842254/a5d2f25db137/pone.0082412.g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/367b/3842254/e63f410d0cc4/pone.0082412.g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/367b/3842254/652e589cba3f/pone.0082412.g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/367b/3842254/3e6762f4b4f8/pone.0082412.g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/367b/3842254/e6cf954df91a/pone.0082412.g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/367b/3842254/a424d7516b67/pone.0082412.g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/367b/3842254/40c5907fcfa6/pone.0082412.g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/367b/3842254/a5d2f25db137/pone.0082412.g007.jpg

相似文献

1
Mild myopathy is associated with COMP but not MATN3 mutations in mouse models of genetic skeletal diseases.轻度肌病与 COMP 相关,但与遗传骨骼疾病的小鼠模型中的 MATN3 突变无关。
PLoS One. 2013 Nov 27;8(11):e82412. doi: 10.1371/journal.pone.0082412. eCollection 2013.
2
A mouse model offers novel insights into the myopathy and tendinopathy often associated with pseudoachondroplasia and multiple epiphyseal dysplasia.一种小鼠模型为假性软骨发育不全症和多发性骨骺发育不良症常伴发的肌肉病和腱病提供了新的见解。
Hum Mol Genet. 2010 Jan 1;19(1):52-64. doi: 10.1093/hmg/ddp466.
3
A novel form of chondrocyte stress is triggered by a COMP mutation causing pseudoachondroplasia.一种新型的软骨细胞应激是由 COMP 突变引起的假性软骨发育不全引起的。
Hum Mutat. 2012 Jan;33(1):218-31. doi: 10.1002/humu.21631. Epub 2011 Nov 17.
4
Genotype to phenotype correlations in cartilage oligomeric matrix protein associated chondrodysplasias.软骨寡聚基质蛋白相关软骨发育不良中的基因型与表型相关性
Eur J Hum Genet. 2014 Nov;22(11):1278-82. doi: 10.1038/ejhg.2014.30. Epub 2014 Mar 5.
5
Pseudoachondroplasia and multiple epiphyseal dysplasia: a 7-year comprehensive analysis of the known disease genes identify novel and recurrent mutations and provides an accurate assessment of their relative contribution.假性软骨发育不全症和多发性骨骺发育不良:对已知疾病基因的 7 年综合分析确定了新的和反复出现的突变,并对其相对贡献进行了准确评估。
Hum Mutat. 2012 Jan;33(1):144-57. doi: 10.1002/humu.21611. Epub 2011 Oct 31.
6
Diverse mutations in the gene for cartilage oligomeric matrix protein in the pseudoachondroplasia-multiple epiphyseal dysplasia disease spectrum.假性软骨发育不全-多发性骨骺发育不良疾病谱中软骨寡聚基质蛋白基因的多种突变。
Am J Hum Genet. 1998 Feb;62(2):311-9. doi: 10.1086/301713.
7
Clinical, Biochemical, Radiological, Genetic and Therapeutic Analysis of Patients with COMP Gene Variants.COMP基因变异患者的临床、生化、放射学、遗传学及治疗分析
Calcif Tissue Int. 2022 Mar;110(3):313-323. doi: 10.1007/s00223-021-00920-6. Epub 2021 Oct 28.
8
COMP mutations, chondrocyte function and cartilage matrix.COMP突变、软骨细胞功能与软骨基质
Matrix Biol. 2005 Jan;23(8):525-33. doi: 10.1016/j.matbio.2004.09.006. Epub 2004 Nov 18.
9
The utility of mouse models to provide information regarding the pathomolecular mechanisms in human genetic skeletal diseases: The emerging role of endoplasmic reticulum stress (Review).小鼠模型在提供人类遗传性骨骼疾病病理分子机制相关信息方面的效用:内质网应激的新作用(综述)
Int J Mol Med. 2015 Jun;35(6):1483-92. doi: 10.3892/ijmm.2015.2158. Epub 2015 Mar 30.
10
Age Dependent Progression of Multiple Epiphyseal Dysplasia and Pseudoachondroplasia Due to Heterozygous Mutations in COMP Gene.由COMP基因突变杂合导致的多发性骨骺发育不良和假性软骨发育不全的年龄依赖性进展
Prague Med Rep. 2020;121(3):153-162. doi: 10.14712/23362936.2020.14.

引用本文的文献

1
Recognizing multiple epiphyseal dysplasia in children presenting with joint pain: a commonly overlooked skeletal dysplasia.认识到关节疼痛儿童中的多发性骨骺发育不良:一种常被忽视的骨骼发育不良。
Eur J Pediatr. 2025 May 20;184(6):350. doi: 10.1007/s00431-025-06176-8.
2
Structure, evolution and expression of zebrafish cartilage oligomeric matrix protein (COMP, TSP5). CRISPR-Cas mutants show a dominant phenotype in myosepta.斑马鱼软骨寡聚基质蛋白(COMP,TSP5)的结构、进化和表达。CRISPR-Cas 突变体在肌膜中表现出显性表型。
Front Endocrinol (Lausanne). 2022 Nov 14;13:1000662. doi: 10.3389/fendo.2022.1000662. eCollection 2022.
3

本文引用的文献

1
Bimodal collagen fibril diameter distributions direct age-related variations in tendon resilience and resistance to rupture.双峰胶原纤维直径分布指导肌腱弹性和抗破裂能力随年龄的变化。
J Appl Physiol (1985). 2012 Sep;113(6):878-88. doi: 10.1152/japplphysiol.00258.2012. Epub 2012 Jul 26.
2
A novel form of chondrocyte stress is triggered by a COMP mutation causing pseudoachondroplasia.一种新型的软骨细胞应激是由 COMP 突变引起的假性软骨发育不全引起的。
Hum Mutat. 2012 Jan;33(1):218-31. doi: 10.1002/humu.21631. Epub 2011 Nov 17.
3
Pseudoachondroplasia and multiple epiphyseal dysplasia: a 7-year comprehensive analysis of the known disease genes identify novel and recurrent mutations and provides an accurate assessment of their relative contribution.
Loss of Smad4 in the scleraxis cell lineage results in postnatal joint contracture.
Smad4 在腱膜纤维细胞谱系中的缺失导致出生后关节挛缩。
Dev Biol. 2021 Feb;470:108-120. doi: 10.1016/j.ydbio.2020.11.006. Epub 2020 Nov 25.
4
Cartilage oligomeric matrix protein: COMPopathies and beyond.软骨寡聚基质蛋白:COMP 病及其他。
Matrix Biol. 2018 Oct;71-72:161-173. doi: 10.1016/j.matbio.2018.02.023. Epub 2018 Mar 9.
5
The utility of mouse models to provide information regarding the pathomolecular mechanisms in human genetic skeletal diseases: The emerging role of endoplasmic reticulum stress (Review).小鼠模型在提供人类遗传性骨骼疾病病理分子机制相关信息方面的效用:内质网应激的新作用(综述)
Int J Mol Med. 2015 Jun;35(6):1483-92. doi: 10.3892/ijmm.2015.2158. Epub 2015 Mar 30.
假性软骨发育不全症和多发性骨骺发育不良:对已知疾病基因的 7 年综合分析确定了新的和反复出现的突变,并对其相对贡献进行了准确评估。
Hum Mutat. 2012 Jan;33(1):144-57. doi: 10.1002/humu.21611. Epub 2011 Oct 31.
4
Development of the musculoskeletal system: meeting the neighbors.肌肉骨骼系统的发育:与邻居相遇。
Development. 2011 Jul;138(14):2855-9. doi: 10.1242/dev.067181.
5
Skeletal dysplasias associated with mild myopathy-a clinical and molecular review.与轻度肌病相关的骨骼发育异常——临床与分子综述
J Biomed Biotechnol. 2010;2010:686457. doi: 10.1155/2010/686457. Epub 2010 May 24.
6
Force transmission between synergistic skeletal muscles through connective tissue linkages.协同骨骼肌之间通过结缔组织连接进行力的传递。
J Biomed Biotechnol. 2010;2010:575672. doi: 10.1155/2010/575672. Epub 2010 Apr 12.
7
Type IX collagen gene mutations can result in multiple epiphyseal dysplasia that is associated with osteochondritis dissecans and a mild myopathy.IX 型胶原基因突变可导致多发性骨骺发育不良,其与剥脱性骨软骨炎和轻度肌病相关。
Am J Med Genet A. 2010 Apr;152A(4):863-9. doi: 10.1002/ajmg.a.33240.
8
Cartilage oligomeric matrix protein promotes cell attachment via two independent mechanisms involving CD47 and alphaVbeta3 integrin.软骨寡聚基质蛋白通过两种涉及 CD47 和 αVβ3 整合素的独立机制促进细胞附着。
Mol Cell Biochem. 2010 May;338(1-2):215-24. doi: 10.1007/s11010-009-0355-3. Epub 2009 Dec 24.
9
BioGPS: an extensible and customizable portal for querying and organizing gene annotation resources.BioGPS:一个可扩展和可定制的门户,用于查询和组织基因注释资源。
Genome Biol. 2009;10(11):R130. doi: 10.1186/gb-2009-10-11-r130. Epub 2009 Nov 17.
10
A mouse model offers novel insights into the myopathy and tendinopathy often associated with pseudoachondroplasia and multiple epiphyseal dysplasia.一种小鼠模型为假性软骨发育不全症和多发性骨骺发育不良症常伴发的肌肉病和腱病提供了新的见解。
Hum Mol Genet. 2010 Jan 1;19(1):52-64. doi: 10.1093/hmg/ddp466.