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肥厚型心肌病患儿的心脏线粒体功能障碍与DNA耗竭

Cardiac mitochondrial dysfunction and DNA depletion in children with hypertrophic cardiomyopathy.

作者信息

Marin-Garcia J, Ananthakrishnan R, Goldenthal M J, Filiano J J, Perez-Atayde A

机构信息

Molecular Cardiology Institute, Highland Park, New Jersey 08904, USA.

出版信息

J Inherit Metab Dis. 1997 Sep;20(5):674-80. doi: 10.1023/a:1005322409330.

Abstract

Abnormalities in specific mitochondrial respiratory enzymes and DNA (mtDNA) have been reported in cardiomyopathy. In this study, we report 4 cases of severe hypertrophic cardiomyopathy (HCM) in which specific cardiac mitochondrial enzyme activity defects were found, including complex I (n = 2), complex III (n = 2), complex IV (n = 2) and complex V (n = 1). Other abnormalities were also noted including a marked depletion of mtDNA (n = 1) and decreased content of subunit 2 of cytochrome c oxidase (n = 1). None of the mtDNA point mutations and common deletions previously found in association with cardiomyopathy were detected in these patients. These data indicate that specific respiratory enzyme activity defects are frequently present in HCM. Also, our finding of a marked depletion of mtDNA in 1 patient suggests that cardiac mtDNA depletion, previously unreported in HCM, needs further examination in order to establish whether it plays a primary role in its pathogenesis.

摘要

心肌病中已报道存在特定线粒体呼吸酶和DNA(mtDNA)异常。在本研究中,我们报告了4例严重肥厚型心肌病(HCM),其中发现了特定的心脏线粒体酶活性缺陷,包括复合体I(n = 2)、复合体III(n = 2)、复合体IV(n = 2)和复合体V(n = 1)。还注意到其他异常,包括mtDNA显著减少(n = 1)和细胞色素c氧化酶亚基2含量降低(n = 1)。在这些患者中未检测到先前发现的与心肌病相关的mtDNA点突变和常见缺失。这些数据表明特定呼吸酶活性缺陷在HCM中经常存在。此外我们在1例患者中发现mtDNA显著减少,这表明心脏mtDNA减少(此前在HCM中未报道)需要进一步研究,以确定其是否在发病机制中起主要作用。

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