Mitochondrial Genome Mutations Associated with Myocardial Infarction

Sazonova, Margarita A.; Рыжкова, А.И.; Sinyov, Vasily V.; Galitsyna, Elena V.; Melnichenko, Alexandra А.; Demakova, Natalya A.; Sobenin, Igor A.; Шкурат, Т. П.; Orekhov, Alexander N.

doi:10.1155/2018/9749457

Cited by 18 publications

(16 citation statements)

References 26 publications

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“…A negative correlation was reported between MI and the variants m.14846G>A and m.12315G>A [10]. It was concluded that the variant m.5178C>A represents a risk factor for the development of MI and that the variants m.14846G>A and m.12315G>A may have a protective effect for MI [10]. In a study of 65 patients with coronary heart disease (CHD) and 23 atherosclerotic plaques, it was found that an mtDNA deletion of 4977 bp was present in 26.2% of the patients as compared to 4.5% in controls [11].…”

Section: Primary Mitochondrial Asclmentioning

confidence: 89%

Section: Primary Mitochondrial Asclmentioning

confidence: 99%

“…In a study of 225 patients with myocardial infarction (MI), a positive correlation between MI and the variant m.5178C>A was found [10]. A negative correlation was reported between MI and the variants m.14846G>A and m.12315G>A [10]. It was concluded that the variant m.5178C>A represents a risk factor for the development of MI and that the variants m.14846G>A and m.12315G>A may have a protective effect for MI [10].…”

Section: Primary Mitochondrial Asclmentioning

confidence: 99%

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Atherosclerosis Can Be Mitochondrial: A Review

Finsterer

2020

Cureus

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One of the systems that are potentially affected in mitochondrial disorders, but hardly get systematically investigated, are the arteries. One of the phenotypic manifestations in arteries is atherosclerosis. This review focuses on the current knowledge and recent advances of mitochondrial atherosclerosis. We conducted a systematic literature review via PubMed using appropriate search terms. Atherosclerosis in mitochondrial disorders may result from a primary pathomechanism or a secondary one due to mitochondrial diabetes, arterial hypertension, or hyperlipidemia. Anecdotal reports show that primary atherosclerosis can be a phenotypic feature of mitochondrial disorders. Predominantly, patients carrying mutations in mtDNA-located genes may develop primary mitochondrial atherosclerosis. Though not systematically investigated, it is conceivable that primary mitochondrial atherosclerosis results from increased oxidative stress, mitophagy, metabolic breakdown, or lactic acidosis. Mitochondrial disorder patients with primary mitochondrial atherosclerosis should receive not only antithrombotic medication but also antioxidants and cofactors. Atherosclerosis in mitochondrial disorders may occur even in the absence of classical atherosclerosis risk factors, suggesting that atherosclerosis can be a primary manifestation of the metabolic defect. Though primary atherosclerosis in mitochondrial disorders has not been systematically investigated, anecdotal data indicate that mitochondrial dysfunction can be a mechanism for the development of primary, mitochondrial atherosclerosis. These patients require antioxidants and cofactors in addition to antithrombotic medication.

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Section: Primary Mitochondrial Asclmentioning

confidence: 89%

Section: Primary Mitochondrial Asclmentioning

confidence: 99%

Section: Primary Mitochondrial Asclmentioning

confidence: 99%

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Atherosclerosis Can Be Mitochondrial: A Review

Finsterer

2020

Cureus

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“…Every year, a large number of people die of it [11,12,13,14,15]. According to the literature, one of the causes of atherosclerosis is mitochondrial dysfunction [16,17,18,19,20]. In particular, the association of atherosclerosis with mitophagy was detected [16,17,18].…”

Section: Introductionmentioning

confidence: 99%

Creation of Cybrid Cultures Containing mtDNA Mutations m.12315G>A and m.1555G>A, Associated with Atherosclerosis

et al. 2019

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In the present work, a pilot creation of four cybrid cultures with high heteroplasmy level was performed using mitochondrial genome mutations m.12315G>A and m.1555G>A. According to data of our preliminary studies, the threshold heteroplasmy level of mutation m.12315G>A is associated with atherosclerosis. At the same time, for a mutation m.1555G>A, such a heteroplasmy level is associated with the absence of atherosclerosis. Cybrid cultures were created by fusion of rho0-cells and mitochondria from platelets with a high heteroplasmy level of the investigated mutations. To create rho0-cells, THP-1 culture of monocytic origin was taken. According to the results of the study, two cybrid cell lines containing mutation m.12315G>A with the heteroplasmy level above the threshold value (25% and 44%, respectively) were obtained. In addition, two cybrid cell lines containing mutation m.1555G>A with a high heteroplasmy level (24%) were obtained. Cybrid cultures with mtDNA mutation m.12315G>A can be used to model both the occurrence and development of atherosclerosis in cells and the titration of drug therapy for patients with atherosclerosis. With the help of cybrid cultures containing single nucleotide replacement of mitochondrial genome m.1555G>A, it is possible to develop approaches to the gene therapy of atherosclerosis.

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“…Myocardial infarction (MI) is 1 of the clinical manifestations of coronary heart disease (CHD). [ 1 ] By 2030, it is estimated 23.3 million will die annually from cardiovascular disease. [ 2 ] ST-segment elevation myocardial infarction (STEMI) is a severe heart attack caused by a prolonged period of blocked blood supply that affects a large area of myocardium and is linked to high incidence of persistent and total coronary occlusion.…”

Section: Introductionmentioning

confidence: 99%