ArticleDisease markers2018
Mitochondrial Genome Mutations Associated with Myocardial Infarction.
Article in Disease markers, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
15 citing papers in PubMed, 27 citations in OpenAlex.
- Article
- Photobiomodulation in cardiovascular diseases: molecular mechanisms and pharmacological approaches to enhance the therapeutics effects of light.Lasers in medical science · 2025Review
- Analysis of Mutational Burden of Mitochondrial Genome in Cells of Different Human Organs and Tissues.Current medicinal chemistry · 2025Review
- Mitochondrial DNA in atherosclerosis research progress: a mini review.Frontiers in immunology · 2025Review
- The two coin sides of bacterial extracellular membrane nanovesicles: atherosclerosis trigger or remedy.Discover nano · 2024Review
- Variability of Mitochondrial DNA Heteroplasmy: Association with Asymptomatic Carotid Atherosclerosis.Biomedicines · 2024Article
- Mitochondrial DNA Is a Vital Driving Force in Ischemia-Reperfusion Injury in Cardiovascular Diseases.Oxidative medicine and cellular longevity · 2022Review
- Mitochondrial Dysfunction in Cardiovascular Diseases: Potential Targets for Treatment.Frontiers in cell and developmental biology · 2022Review
- Protective effects of 18β-Glycyrrhetinic acid against myocardial infarction: Involvement of PI3K/Akt pathway activation and inhibiting CaFood science & nutrition · 2021Article
- Mitochondrial Lipid Homeostasis at the Crossroads of Liver and Heart Diseases.International journal of molecular sciences · 2021Review
- The Diseased Mitoribosome.FEBS letters · 2021Review
- Some Molecular and Cellular Stress Mechanisms Associated with Neurodegenerative Diseases and Atherosclerosis.International journal of molecular sciences · 2021Review
- Natural Antioxidants Improve the Vulnerability of Cardiomyocytes and Vascular Endothelial Cells under Stress Conditions: A Focus on Mitochondrial Quality Control.Oxidative medicine and cellular longevity · 2021Review
- Atherosclerosis Can Be Mitochondrial: A Review.Cureus · 2020Review
- Creation of Cybrid Cultures Containing mtDNA Mutations m.12315G>A and m.1555G>A, Associated with Atherosclerosis.Biomolecules · 2019Article
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Myocardial infarction is one of the clinical manifestations of coronary heart disease. In some cases, the cause of myocardial infarction may be atherosclerotic plaques which occurred in the human aorta. The association of mtDNA mutations with atherosclerotic lesions in human arteries was previously detected by our research group. In this study, we used samples of white blood cells collected from 225 patients with myocardial infarction and 239 control persons with no health complaints. DNA was isolated from the blood leukocyte samples. Then, PCR fragments of DNA were obtained. They contained the investigated regions of 11 mitochondrial genome mutations (m.5178C>A, m.3336T>C, m.652delG, m.12315G>A, m.14459G>A, m.652insG, m.14846G>A, m.13513G>A, m.1555A>G, m.15059G>A, m.3256C>T). According to the obtained results, three mutations of the human mitochondrial genome correlated with myocardial infarction. A positive correlation was observed for mutation m.5178C>A. At the same time, a highly significant negative correlation with myocardial infarction was observed for mutation m.14846G>A. One single-nucleotide substitution of m.12315G>A had a trend towards negative correlation. These mutations can potentially be useful for creating molecular/cellular models for studying the mechanisms of myocardial infarction and designing novel therapies. Moreover, these mutations can possibly be used for diagnostic purposes.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.