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线粒体单倍群可改变丹麦人群患肥厚型心肌病的风险。

Mitochondrial haplogroups modify the risk of developing hypertrophic cardiomyopathy in a Danish population.

机构信息

Department of Clinical Biochemistry and Immunology, Statens Serum Institut, Copenhagen, Denmark.

出版信息

PLoS One. 2013 Aug 5;8(8):e71904. doi: 10.1371/journal.pone.0071904. Print 2013.

Abstract

Hypertrophic cardiomyopathy (HCM) is a genetic disorder caused by mutations in genes coding for proteins involved in sarcomere function. The disease is associated with mitochondrial dysfunction. Evolutionarily developed variation in mitochondrial DNA (mtDNA), defining mtDNA haplogroups and haplogroup clusters, is associated with functional differences in mitochondrial function and susceptibility to various diseases, including ischemic cardiomyopathy. We hypothesized that mtDNA haplogroups, in particular H, J and K, might modify disease susceptibility to HCM. Mitochondrial DNA, isolated from blood, was sequenced and haplogroups identified in 91 probands with HCM. The association with HCM was ascertained using two Danish control populations. Haplogroup H was more prevalent in HCM patients, 60% versus 46% (p = 0.006) and 41% (p = 0.003), in the two control populations. Haplogroup J was less prevalent, 3% vs. 12.4% (p = 0.017) and 9.1%, (p = 0.06). Likewise, the UK haplogroup cluster was less prevalent in HCM, 11% vs. 22.1% (p = 0.02) and 22.8% (p = 0.04). These results indicate that haplogroup H constitutes a susceptibility factor and that haplogroup J and haplogroup cluster UK are protective factors in the development of HCM. Thus, constitutive differences in mitochondrial function may influence the occurrence and clinical presentation of HCM. This could explain some of the phenotypic variability in HCM. The fact that haplogroup H and J are also modifying factors in ischemic cardiomyopathy suggests that mtDNA haplotypes may be of significance in determining whether a physiological hypertrophy develops into myopathy. mtDNA haplotypes may have the potential of becoming significant biomarkers in cardiomyopathy.

摘要

肥厚型心肌病(HCM)是一种由编码肌节蛋白的基因突变引起的遗传疾病。该疾病与线粒体功能障碍有关。线粒体 DNA(mtDNA)的进化发展变异,定义了 mtDNA 单倍群和单倍群簇,与线粒体功能的功能差异和对各种疾病的易感性相关,包括缺血性心肌病。我们假设 mtDNA 单倍群,特别是 H、J 和 K,可能会改变 HCM 的疾病易感性。从血液中分离出 mtDNA 并进行测序,鉴定 91 名 HCM 先证者的单倍群。使用两个丹麦对照人群来确定与 HCM 的关联。HCM 患者中 H 单倍群更为常见,分别为 60%与 46%(p = 0.006)和 41%(p = 0.003),而在两个对照人群中。J 单倍群则较少见,分别为 3%与 12.4%(p = 0.017)和 9.1%(p = 0.06)。同样,UK 单倍群簇在 HCM 中也较少见,分别为 11%与 22.1%(p = 0.02)和 22.8%(p = 0.04)。这些结果表明,H 单倍群构成了一个易感因素,而 J 单倍群和 UK 单倍群簇则是 HCM 发展的保护因素。因此,线粒体功能的组成差异可能会影响 HCM 的发生和临床表现。这可以解释 HCM 中的一些表型变异性。H 单倍群和 J 单倍群也是缺血性心肌病的修饰因子这一事实表明,mtDNA 单倍型可能在决定生理性肥大是否发展为肌病方面具有重要意义。mtDNA 单倍型可能具有成为心肌病重要生物标志物的潜力。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5dc7/3734310/7134e3ca0285/pone.0071904.g001.jpg

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