ArticleClinical & developmental immunology2012
Mitochondrial mutations are associated with atherosclerotic lesions in the human aorta.
Article in Clinical & developmental immunology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
40 citing papers in PubMed, 64 citations in OpenAlex.
- Skin as a sentinel and modulator of systemic aging: a translational framework for evidence-based gerotherapeutics.GeroScience · 2026Review
- Changes to small RNA expression in macrophages in response to very low-density lipoprotein lipid hydrolysis by lipoprotein lipase and NADPH oxidase inhibition.BMC research notes · 2026Article
- Mechanisms of Inflammation Chronification: Gene and Epigenetic Regulation of Intolerant Response (Trained Immunity).Current medicinal chemistry · 2026Article
- Mitochondrial Dysfunction Associated with mtDNA Mutation: Mitochondrial Genome Editing in Atherosclerosis Research.Current medicinal chemistry · 2026Article
- Relationship between Cellular Oxygen Consumption and Atherosclerosis-associated Mitochondrial Mutations (Variants of the Mitochondrial Genome).Current medicinal chemistry · 2026Article
- The Role of mtDNA Mutations in Atherosclerosis: The Influence of Mitochondrial Dysfunction on Macrophage Polarization.International journal of molecular sciences · 2025Review
- Defective Mitophagy Impairs Response to Inflammatory Activation of Macrophage-Like Cells.Current medicinal chemistry · 2025Article
- Two Sides of Triglycerides in Atherogenesis: An Essential Contributor.Clinical Medicine Insights. Cardiology · 2025Review
- The role of mitochondria-related genes and immune infiltration in carotid atherosclerosis: identification of hub targets through bioinformatics and machine learning approaches.Frontiers in genetics · 2025Article
- TMAO Induces Vascular Endothelial Cells Pyroptosis Through TET2-CYTB-ROS Pathway.Journal of inflammation research · 2025Article
- Atherosclerosis originating from childhood: Specific features.Journal of biomedical research · 2024Article
- The Mitochondrial m.3243A>G Mutation on the Dish, Lessons from In Vitro Models.International journal of molecular sciences · 2023Review
- Creation of Mitochondrial Disease Models Using Mitochondrial DNA Editing.Biomedicines · 2023Review
- Diagnostics of atherosclerosis: Overview of the existing methods.Frontiers in cardiovascular medicine · 2023Review
- From Diabetes to Atherosclerosis: Potential of Metformin for Management of Cardiovascular Disease.International journal of molecular sciences · 2022Review
- The Role of Mitochondrial Abnormalities in Diabetic Cardiomyopathy.International journal of molecular sciences · 2022Review
- Effects of Metabolic Disorders in Immune Cells and Synoviocytes on the Development of Rheumatoid Arthritis.Metabolites · 2022Review
- Role of Impaired Mitochondrial Dynamics Processes in the Pathogenesis of Alzheimer's Disease.International journal of molecular sciences · 2022Review
- Aging of Vascular System Is a Complex Process: The Cornerstone Mechanisms.International journal of molecular sciences · 2022Review
- Somatic Mutations in Cardiovascular Disease.Circulation research · 2022Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Somatic mutations of the human mitochondrial genome can be a possible determinant of atherosclerosis. To test this possibility, forty mitochondrial mutations were analyzed in the present study in order to see which of these mutations might be associated with atherosclerosis. Ten mitochondrial mutations belonging to mitochondrial genes MT-RNR1 (rRNA 12S); MT-TL1 (tRNA-Leu, recognizes UUR); MT-TL2 (tRNA-Leu, recognizes CUN); MT-ND1, MT-ND2, MT-ND5, and MT-ND6 (subunits 1, 2, 5, and 6, respectively, of NADH dehydrogenase); and MT-CYB (cytochrome b) were potentially associated with atherosclerosis. From 29% (2 of 7 aortic samples) upto 86% (6 of 7 aortic samples) of aortic samples had a significant difference between atherosclerotic plaques and unaffected tissue, with the respect to the level of heteroplasmy for each mutation. Further, the homogenates of affected and normal intimae of 22 aortas were compared to reveal the average level of heteroplasmy for the above-mentioned 10 mutations. For five mutations, the mean level of heteroplasmy was significantly different in atherosclerotic intimal homogenates in comparison with the unaffected tissue. These mutations were A1555G, C3256T, T3336C, G13513A, and G15059A. Thus, it was demonstrated that at least five mitochondrial mutations occurring in MT-RNR1, MT-TL1, MT-ND2, MT-ND5, and MT-CYB genes are associated with atherosclerosis.
Indexed as
Identifiers
What OpenQuestion holds
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.