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在人类心肌病症中分离的线粒体生物发生反应

Preeti Ahuja¹, Jonathan Wanagat, Zhihua Wang

¹Department of Anesthesiology, Division of Molecular Medicine, David Geffen School of Medicine at UCLA, BH-569 CHS, BOX 957115, Los Angeles, CA 90095, USA. Pahuja@mednet.ucla.edu

|April 17, 2013

概括

心力衰竭中的线粒体功能障碍与DNA损伤和缺失有关,特别是在扩张性心肌病症中. 这表明有缺陷的补偿反应加剧了氧化应激.

科学领域:

心脏病学心脏病学
线粒体生物学线粒体生物学
遗传学是一个遗传学.

背景情况:

线粒体在心力衰竭 (HF) 发病过程中起着至关重要的作用.
线粒体功能障碍会损害能量生产,促进细胞死亡,加剧左心室衰竭.
在HF中线粒体功能障碍的确切机制仍然不清楚.

研究的目的:

在人类心力衰竭中调查线粒体形态,生物发生和基因组完整性.
为了比较心脏不衰竭,缺血性心肌病 (ICM) 和扩张性心肌病 (DCM) 的线粒体特征.

主要方法:

来自不衰竭,ICM和DCM心脏的左心室组织的分析.
评估线粒体形态,数量,体积密度和mtDNA拷贝数.
评估mtDNA编码的基因表达,mtDNA修复和抗氧化剂基因表达.
量化mtDNA删除突变的量化.

主要成果:

在ICM和DCM中观察到线粒体功能障碍.
与ICM相比,DCM心脏的线粒体较小,数量更多,体积密度增加,mtDNA复制数增加.
在DCM中增加mtDNA编码基因的表达,但在失败的心脏中减少mtDNA修复和抗氧化基因表达.
在DCM心脏中发现mtDNA删除突变的显著增加.

结论:

在DCM中,线粒体功能障碍与mtDNA损伤和缺失有关.
这可能是由于突变性压力和线粒体生物发生的补偿性增加造成的.
这种反应似乎是不适应的,增加了氧化损伤,并强调了对DCM线粒体功能障碍的新治疗策略的需要.

关键词:

这些都是DNA,线粒体DNA.心肌病,扩大心肌病,扩大心肌病.心脏衰竭是因为心脏衰竭.线粒体的周转率

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