ArticleScientific reports2018
Analysis of mitochondrial function in human induced pluripotent stem cells from patients with mitochondrial diabetes due to the A3243G mutation.
Article in Scientific reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed.
- Patient specific regulation of metabolism and cell death pathways in m.3243A>G mutated iPS-cells.Scientific reports · 2026Article
- Impaired mitochondrial morphology and respiratory dysfunction in human induced pluripotent stem cells with mitochondrial tRNA mutations (m.3243A>G and m.14739G>A).Orphanet journal of rare diseases · 2026Article
- Mitochondrial DNA variation and intervertebral disc degeneration: a genotypic analysis in a South African cohort.Molecular biology reports · 2025Article
- Retinal multimodal-imaging and functional tests in a mitochondrial disease with focal and segmental glomerulosclerosis.International journal of ophthalmology · 2025Review
- The Mitochondrial m.3243A>G Mutation on the Dish, Lessons from In Vitro Models.International journal of molecular sciences · 2023Review
- Clinical and molecular features of two diabetes families carrying mitochondrial ND1 T3394C mutation.Irish journal of medical science · 2022Article
- A PI polyamide-TPP conjugate targeting a mtDNA mutation induces cell death of cancer cells with the mutation.Cancer science · 2021Article
- Mitochondrial DNA Dynamics in Reprogramming to Pluripotency.Trends in cell biology · 2021Review
- Pressure-Driven Mitochondrial Transfer Pipeline Generates Mammalian Cells of Desired Genetic Combinations and Fates.Cell reports · 2020Article
- Cell models and drug discovery for mitochondrial diseases.Journal of Zhejiang University. Science. B · 2019Review
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Authors and funding
8 authors.
Funding
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Abstract
We previously established human induced pluripotent stem (iPS) cells in two diabetic patients from different families with the mitochondrial A3243G mutation and isolated isogenic iPS cell clones with either undetectable or high levels of the mutation in both patients. In the present study, we analyzed the mitochondrial functions of two mutation-undetectable and two mutation-high clones in each patient through four methods to assess complex I activity, mitochondrial membrane potential, mitochondrial respiration, and mitochondrial ATP production. In the first patient, complex I activity, mitochondrial respiration, and mitochondrial ATP production were decreased in the mutation-high clones compared with the mutation-undetectable clones, and mitochondrial membrane potential was decreased in a mutation-high clone compared with a mutation-undetectable clone. In the second patient, complex I activity was decreased in one mutation-high clone compared with the other clones. The other parameters showed no differences in any clones. In addition, the complex I activity and mitochondrial respiration of the mutation-undetectable clones from both patients were located in the range of those of iPS cells from healthy subjects. The present study suggests that the mitochondrial function of the mutation-undetectable iPS cell clones obtained from two patients with the A3243G mutation is comparable to the control iPS cells.
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