Association of mitochondrial DNA polymorphism with myocardial infarction and prognostic signs for atherosclerosis

被引:0
作者
M. V. Golubenko
R. R. Salakhov
O. A. Makeeva
I. A. Goncharova
V. V. Kashtalap
O. L. Barbarash
V. P. Puzyrev
机构
[1] Research Institute for Medical Genetics,
[2] Research Institute for Complex Issues of Cardiovascular Diseases,undefined
[3] National Research Tomsk State University,undefined
来源
Molecular Biology | 2015年 / 49卷
关键词
mitochondrial DNA; genetic polymorphism; myocardial infarction;
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摘要
We performed an association analysis for the mtDNA major common variants and haplogroups with incidence of myocardial infarction and essential prognostic characteristics in patients. A comparison of patients (N = 406) and control groups (N = 183) uncovered a higher frequency of HV0 haplogroup in patients (6.9% vs. 2.2%; p = 0.033). Patients with early infarction (before age of 55 in men) had a higher frequency of 16189C variant, compared to patients who endured first infarction at age older than 55 (24.1% vs. 12.5%; p = 0.008). In addition, haplogroup U2e was only detected in the subgroup with early infarction (4.4%; p = 0.004). Haplogroup U5 was less frequent in patients with early infarction (5.1% vs. 15.4%; p = 0.002). Observations during a 1-year follow-up uncovered that patients with recurring cardiovascular incidents had higher frequency of haplogroup H1 (20%, versus 4.5% in patients without complications, p = 0.002) and variant 16189C (30% versus 13.5%; p = 0.018). Haplogroup U5 was more frequent in the subgroup of patients with lower (<40%) ventricular ejection fraction (17.1%, compared to 8.2%; p = 0.034). Thus, our results indicate that mtDNA polymorphism contributes to coronary atherosclerosis. The obtained associations can be explained by the effect of polymorphisms on oxidative phosphorylation and the production of reactive oxygen species in mitochondria.
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页码:867 / 874
页数:7
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共 215 条
[11]  
Logan A.(1967)Treatment of myocardial infarction in a coronary care unit a two year experience with 250 patients Am. J. Cardiol 20 457-464
[12]  
West N.E.J.(1995)Demographic history of India and mtDNA-sequence diversity Am. J. Hum. Genet 56 979-992
[13]  
Clarke M.C.H.(1999)BioEdit: A user-friendly biological sequence alignment editor and analysis program for Windows 95/98/NT Nucl. Acids. Symp. Ser 41 95-98
[14]  
Vidal-Puig A.(1996)Classification of European mtDNAs from an analysis of three European populations Genetics 144 1835-1850
[15]  
Murphy M.P.(1997)A common mtDNA polymorphism associated with variation in plasma triglyceride concentration Am. J. Hum. Genet 60 1552-1555
[16]  
Bennett M.R.(1999)Association of polymorphism in non-coding regions of the human mitochondrial genome with blood pressure variability and ECG intervals Bull. Exp. Biol. Med 127 82-84
[17]  
Wallace D.C.(2001)Analysis of a polycytosine tract and heteroplasmic length variation in the mitochondrial DNA D-loop of patients with diabetes, MELAS syndrome and race-matched controls Diabet. Med 18 413-416
[18]  
Sena L.A.(2013)The association of the mitochondrial DNA OriB variant (16184–16193 polycytosine tract) with type 2 diabetes in Europid populations Diabetologia 56 1907-1913
[19]  
Chandel N.S.(2005)Mitochondrial DNA polymorphism in Russian population form five oblasts of the European part of Russia Russ. J. Genet 41 1040-1045
[20]  
Gutierrez J.(2002)Type 2 diabetes is associated with a common mitochondrial variant: Evidence from a population-based case-control study Hum. Mol. Genet 11 1581-1583