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1
Attenuated mitochondrial NADP+-dependent isocitrate dehydrogenase activity induces apoptosis and hypertrophy of H9c2 cardiomyocytes.线粒体 NADP+-依赖性异柠檬酸脱氢酶活性减弱诱导 H9c2 心肌细胞凋亡和肥大。
Biochimie. 2014 Apr;99:110-8. doi: 10.1016/j.biochi.2013.11.016. Epub 2013 Dec 1.
2
Mitochondrial morphology-emerging role in bioenergetics.线粒体形态在生物能量学中的新兴作用。
Free Radic Biol Med. 2012 Dec 15;53(12):2218-28. doi: 10.1016/j.freeradbiomed.2012.09.035. Epub 2012 Sep 29.
3
Signal transduction by reactive oxygen species.活性氧物种的信号转导。
J Cell Biol. 2011 Jul 11;194(1):7-15. doi: 10.1083/jcb.201102095.
4
Mitochondrial adaptations to physiological vs. pathological cardiac hypertrophy.线粒体对生理性和病理性心肌肥厚的适应。
Cardiovasc Res. 2011 May 1;90(2):234-42. doi: 10.1093/cvr/cvr015. Epub 2011 Jan 21.
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Oxidation of myofibrillar proteins in human heart failure.肌原纤维蛋白在人类心力衰竭中的氧化。
J Am Coll Cardiol. 2011 Jan 18;57(3):300-9. doi: 10.1016/j.jacc.2010.06.058.
6
Therapeutic targeting of mitochondrial superoxide in hypertension.高血压中线粒体超氧化物的治疗靶向。
Circ Res. 2010 Jul 9;107(1):106-16. doi: 10.1161/CIRCRESAHA.109.214601. Epub 2010 May 6.
7
The cell cycle is a redox cycle: linking phase-specific targets to cell fate.细胞周期是一个氧化还原循环：将特定阶段的靶点与细胞命运联系起来。
Free Radic Biol Med. 2009 Nov 1;47(9):1282-93. doi: 10.1016/j.freeradbiomed.2009.05.026. Epub 2009 May 29.
8
Copper reverses cardiomyocyte hypertrophy through vascular endothelial growth factor-mediated reduction in the cell size.铜通过血管内皮生长因子介导的细胞大小减小来逆转心肌细胞肥大。
J Mol Cell Cardiol. 2008 Jul;45(1):106-17. doi: 10.1016/j.yjmcc.2008.03.022. Epub 2008 Apr 9.
9
Mitochondrial fission mediates high glucose-induced cell death through elevated production of reactive oxygen species.线粒体分裂通过增加活性氧的产生介导高糖诱导的细胞死亡。
Cardiovasc Res. 2008 Jul 15;79(2):341-51. doi: 10.1093/cvr/cvn104. Epub 2008 Apr 25.
10
Hydrogen peroxide as an endogenous mediator and exogenous tool in cardiovascular research: issues and considerations.过氧化氢作为心血管研究中的内源性介质和外源性工具：问题与思考
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异柠檬酸脱氢酶2（IDH2）的下调加剧了血红素加氧酶（HO）介导的细胞死亡和肥大。

Downregulation of IDH2 exacerbates HO-mediated cell death and hypertrophy.

作者信息

Ku Hyeong Jun, Park Jeen-Woo

机构信息

a School of Life Sciences and Biotechnology, BK21 Plus KNU Creative BioResearch Group , Kyungpook National University , Taegu , Korea.

出版信息

Redox Rep. 2017 Jan;22(1):35-41. doi: 10.1080/13510002.2015.1135581. Epub 2016 Feb 15.

DOI:10.1080/13510002.2015.1135581
PMID:26865387
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6837399/
Abstract

OBJECTIVES

Reactive oxygen species-mediated cell death contributes to the pathophysiology of cardiovascular disease and myocardial dysfunction. We recently showed that mitochondrial NADP-dependent isocitrate dehydrogenase (IDH2) functions as an antioxidant and anti-apoptotic protein by supplying NADPH to antioxidant systems.

METHODS

In the present study, we demonstrated that HO-induced apoptosis and hypertrophy of H9c2 cardiomyoblasts was markedly exacerbated by small interfering RNA (siRNA) specific for IDH2.

RESULTS

Attenuated IDH2 expression resulted in the modulation of cellular and mitochondrial redox status, mitochondrial function, and cellular oxidative damage. MitoTEMPO, a mitochondria-targeted antioxidant, efficiently suppressed increased caspase-3 activity, increased cell size, and depletion of cellular GSH levels in IDH2 siRNA-transfected cells that were treated with HO.

DISCUSSION

These results indicated that the disruption of cellular redox balance might be responsible for the enhanced HO-induced apoptosis and hypertrophy of cultured cardiomyocytes by the attenuated IDH2 expression.

摘要

目的

活性氧介导的细胞死亡参与心血管疾病和心肌功能障碍的病理生理过程。我们最近发现，线粒体烟酰胺腺嘌呤二核苷酸磷酸（NADP）依赖性异柠檬酸脱氢酶2（IDH2）通过为抗氧化系统提供还原型辅酶II（NADPH）发挥抗氧化和抗凋亡蛋白的作用。

方法

在本研究中，我们证明，IDH2特异性小干扰RNA（siRNA）显著加剧了过氧化氢（HO）诱导的H9c2心肌成纤维细胞凋亡和肥大。

结果

IDH2表达减弱导致细胞和线粒体氧化还原状态、线粒体功能以及细胞氧化损伤的改变。线粒体靶向抗氧化剂MitoTEMPO有效抑制了HO处理的IDH2 siRNA转染细胞中半胱天冬酶-3活性增加、细胞大小增加以及细胞内谷胱甘肽（GSH）水平降低。

讨论

这些结果表明，细胞氧化还原平衡的破坏可能是IDH2表达减弱导致HO诱导的培养心肌细胞凋亡和肥大增强的原因。