ArticleMitochondrion2018
Relations of mitochondrial genetic variants to measures of vascular function.
Article in Mitochondrion, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
What it found
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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.
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.
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Who cites it
5 citing papers in PubMed.
- The PVAT-MAMs Axis in Atherosclerosis: A Hypothesis-Driven Cross-Scale Conceptual Framework.International journal of molecular sciences · 2026Review
- Arterial stiffness and vascular aging: mechanisms, prevention, and therapy.Signal transduction and targeted therapy · 2025Review
- Lessons from the deep: mechanisms behind diversification of eukaryotic protein complexes.Biological reviews of the Cambridge Philosophical Society · 2023Article
- Analysis of functional variants in mitochondrial DNA of Finnish athletes.BMC genomics · 2019Article
- Associations of Mitochondrial and Nuclear Mitochondrial Variants and Genes with Seven Metabolic Traits.American journal of human genetics · 2019Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors.
Funding
Abstract
Mitochondrial genetic variation with resultant alterations in oxidative phosphorylation may influence vascular function and contribute to cardiovascular disease susceptibility. We assessed relations of peptide-encoding variants in the mitochondrial genome with measures of vascular function in Framingham Heart Study participants. Of 258 variants assessed, 40 were predicted to have functional consequences by bioinformatics programs. A maternal pattern of heritability was estimated to contribute to the variability of aortic stiffness. A putative association with a microvascular function measure was identified that requires replication. The methods we have developed can be applied to assess the relations of mitochondrial genetic variation to other phenotypes.
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Registered trials
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