ArticleAging2016
Study of mitochondrial respiratory defects on reprogramming to human induced pluripotent stem cells.
Article in Aging, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 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
25 citing papers in PubMed.
- Long-read sequencing-based atlas of tissue-specific expression of DNM1L transcript variants.The FEBS journal · 2026Article
- Advances in diagnosis of mitochondrial dysfunction and primary mitochondrial disease.Disease models & mechanisms · 2026Review
- Article
- Mitochondria and pluripotency: from established models to emerging roles in adult stem cells.Frontiers in bioengineering and biotechnology · 2025Review
- Maculopapillary Bundle Degeneration in Optic Neuropathies.Current neurology and neuroscience reports · 2024Review
- Development of a CRISPRi Human Retinal Pigmented Epithelium Model for Functional Study of Age-Related Macular Degeneration Genes.International journal of molecular sciences · 2023Article
- iPSC culture expansion selects against putatively actionable mutations in the mitochondrial genome.Stem cell reports · 2021Article
- Modelling Mitochondrial Disease in Human Pluripotent Stem Cells: What Have We Learned?International journal of molecular sciences · 2021Review
- Mitochondrial DNA Dynamics in Reprogramming to Pluripotency.Trends in cell biology · 2021Review
- Review
- Exploiting hiPSCs in Leber's Hereditary Optic Neuropathy (LHON): Present Achievements and Future Perspectives.Frontiers in neurology · 2021Article
- Strategies for Cancer Immunotherapy Using Induced Pluripotency Stem Cells-Based Vaccines.Cancers · 2020Review
- Neuronal Reprogramming for Tissue Repair and Neuroregeneration.International journal of molecular sciences · 2020Review
- Emerging model systems and treatment approaches for Leber's hereditary optic neuropathy: Challenges and opportunities.Biochimica et biophysica acta. Molecular basis of disease · 2020Review
- Generation of a Transplantable Population of Human iPSC-Derived Retinal Ganglion Cells.Frontiers in cell and developmental biology · 2020Article
- Episomal Induced Pluripotent Stem Cells: Functional and Potential Therapeutic Applications.Cell transplantation · 2019Review
- Mitochondrial fission protein Drp1 inhibition promotes cardiac mesodermal differentiation of human pluripotent stem cells.Cell death discovery · 2018Article
- The functional genomics laboratory: functional validation of genetic variants.Journal of inherited metabolic disease · 2018Review
- Pluripotent Stem Cell-Based Approaches to Explore and Treat Optic Neuropathies.Frontiers in neuroscience · 2018Review
- Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
11 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Reprogramming of somatic cells into a pluripotent state is known to be accompanied by extensive restructuring of mitochondria and switch in metabolic requirements. Here we utilized Leber's hereditary optic neuropathy (LHON) as a mitochondrial disease model to study the effects of homoplasmic mtDNA mutations and subsequent oxidative phosphorylation (OXPHOS) defects in reprogramming. We obtained fibroblasts from a total of 6 LHON patients and control subjects, and showed a significant defect in complex I respiration in LHON fibroblasts by high-resolution respiratory analysis. Using episomal vector reprogramming, our results indicated that human induced pluripotent stem cell (hiPSC) generation is feasible in LHON fibroblasts. In particular, LHON-specific OXPHOS defects in fibroblasts only caused a mild reduction and did not significantly affect reprogramming efficiency, suggesting that hiPSC reprogramming can tolerate a certain degree of OXPHOS defects. Our results highlighted the induction of genes involved in mitochondrial biogenesis (TFAM, NRF1), mitochondrial fusion (MFN1, MFN2) and glycine production (GCAT) during reprogramming. However, LHON-associated OXPHOS defects did not alter the kinetics or expression levels of these genes during reprogramming. Together, our study provides new insights into the effects of mtDNA mutation and OXPHOS defects in reprogramming and genes associated with various aspects of mitochondrial biology.
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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.