Level of blood cell-free circulating mitochondrial DNA as a novel biomarker of acute myocardial ischemia

被引:0
作者
N. P. Sudakov
T. P. Popkova
A. I. Katyshev
O. A. Goldberg
S. B. Nikiforov
B. G. Pushkarev
I. V. Klimenkov
S. A. Lepekhova
K. A. Apartsin
G. A. Nevinsky
Yu. M. Konstantinov
机构
[1] Irkutsk Surgery and Traumatology Research Center,Irkutsk Research Center
[2] Irkutsk State University,Siberian Institute of Plant Physiology and Biochemistry
[3] Siberian Branch of the Russian Academy of Sciences,Limnological Institute
[4] Siberian Branch of the Russian Academy of Sciences,Institute of Chemical Biology and Fundamental Medicine
[5] Siberian Branch of the Russian Academy of Sciences,undefined
[6] Siberian Branch of the Russian Academy of Sciences,undefined
来源
Biochemistry (Moscow) | 2015年 / 80卷
关键词
acute ischemic myocardial injury; cell-free circulating mtDNA; cytolysis biomarkers; real-time PCR;
D O I
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中图分类号
学科分类号
摘要
Changes in the level of blood cell-free circulating mitochondrial DNA were examined during experimental adrenaline-induced myocardial injury in rats. The amount of mitochondrial DNA in the blood was significantly elevated at 48 and 72 h after subcutaneous injection of adrenaline solution, and it was accompanied by development of multiple smallfocal myocardial ischemia. This suggests that the measured level of blood cell-free circulating mitochondrial DNA might be used as a biomarker of acute myocardial ischemia.
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页码:1387 / 1392
页数:5
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[1]  
Thygesen K.(2012)Writing group on behalf of the joint ESC/ACCF/AHA/WHF task force for the universal definition of myocardial infarction. Third universal definition of myocardial infarction J. Am. Coll. Cardiol 60 1581-1598
[2]  
Alpert J. S.(2015)Distinct mPTP activation mechanisms in ischemia-reperfusion: contributions of Ca Cardiovasc. Res 106 237-248
[3]  
Jaffe A. S.(2013), ROS, pH, and inorganic polyphos-phate Arch. Med. Sci 9 968-975
[4]  
Simoons M. L.(2014)Infarct size reduction by cyclosporine A at reperfusion involves inhibition of the mitochondrial permeability transition pore but does not improve mitochondrial respiration Redox Biol 2 702-714
[5]  
Chaitman B. R.(2004)Mitochondrial reactive oxygen species: a double-edged sword in ischemia/reperfusion vs preconditioning Scienc 305 626-662
[6]  
White H. D.(2004)The pathophysiolo-gy of mitochondrial cell death Cell Mol. Life Sci 61 3100-3103
[7]  
Seidlmayer L. K.(2006)Mitochondrial perme-ability transition triggers the release of mtDNA fragments Mitochondrio 6 43-47
[8]  
Juettner V. V.(2007)Release of mito-chondrial DNA fragments from brain mitochondria of irra-diated mice Life Sci 81 1160-1166
[9]  
Kettlewell S.(2003)Mitochondrial DNA fragments released through the permeability transition pore correspond to specific gene size Clin. Chim. Act 327 95-101
[10]  
Pavlov E. V.(2008)Elevated cell-free serum DNA detected in patients with myocardial infarction BJU Int 102 628-632