Suppr超能文献

肌病与大规模线粒体DNA重复和缺失的关联:何者具有致病性?

Association of myopathy with large-scale mitochondrial DNA duplications and deletions: which is pathogenic?

作者信息

Manfredi G, Vu T, Bonilla E, Schon E A, DiMauro S, Arnaudo E, Zhang L, Rowland L P, Hirano M

机构信息

H. Houston Merritt Clinical Research Center for Muscular Dystrophy and Related Disorders, and Department of Neurology, Columbia University College of Physicians and Surgeons, New York, NY 10032, USA.

出版信息

Ann Neurol. 1997 Aug;42(2):180-8. doi: 10.1002/ana.410420208.

Abstract

We identified large-scale heteroplasmic mitochondrial DNA (mtDNA) rearrangements in a 50-year-old woman with an adult-onset progressive myopathy. The predominant mtDNA abnormality was a 21.2-kb duplicated molecule. In addition, a small population of the corresponding partially deleted 4.6-kb molecule was detected. Skeletal muscle histology revealed fibers that were negative for cytochrome c oxidase (COX) activity and had reduced mtDNA-encoded COX subunits. By single-fiber polymerase chain reaction analysis, COX-negative fibers contained a low number of wild-type or duplicated mtDNA molecules (ie, nondeleted). In situ hybridization demonstrated that the abnormal fibers contained increased amounts of mtDNA compared with normal fibers and that most of the genomes were deleted. We concluded that deleted mtDNA molecules were primarily responsible for the phenotype in this patient.

摘要

我们在一名患有成人起病的进行性肌病的50岁女性中发现了大规模异质性线粒体DNA(mtDNA)重排。主要的mtDNA异常是一个21.2 kb的重复分子。此外,还检测到一小部分相应的部分缺失的4.6 kb分子。骨骼肌组织学显示,细胞色素c氧化酶(COX)活性阴性的纤维,其mtDNA编码的COX亚基减少。通过单纤维聚合酶链反应分析,COX阴性纤维中野生型或重复的mtDNA分子数量较少(即未缺失)。原位杂交表明,与正常纤维相比,异常纤维中mtDNA含量增加,且大多数基因组被删除。我们得出结论,缺失的mtDNA分子是该患者表型的主要原因。

文献AI研究员

20分钟写一篇综述,助力文献阅读效率提升50倍。

立即体验

用中文搜PubMed

大模型驱动的PubMed中文搜索引擎

马上搜索

文档翻译

学术文献翻译模型,支持多种主流文档格式。

立即体验