ArticleEMBO molecular medicine2020
Disease-specific phenotypes in iPSC-derived neural stem cells with POLG mutations.
Article in EMBO molecular medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers, 2 of them syntheses that pooled it.
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
41 citing papers in PubMed, 2 syntheses or guidelines pooled it, 58 citations in OpenAlex.
- Modelling mitochondrial diseases in neuronsJournal of neuromuscular diseases · 2025Pooled it
- Model systems informing mechanisms and drug discovery: a review ofWellcome open research · 2023Pooled it
- The role of impaired mitochondrial function in neurological manifestations of mitochondrial diseases.Mammalian genome : official journal of the International Mammalian Genome Society · 2026Review
- Impaired NADH-linked mitochondrial respiration disrupts ventral midbrain neuronal programs in POLG disease.Journal of translational medicine · 2026Article
- Genetic contributions to mitochondrial dysfunction in amyotrophic lateral sclerosis etiology.HGG advances · 2026Article
- The Mitochondrial Guardian α-Amyrin Mitigates Alzheimer's Disease Pathology via Modulation of the DLK-SARM1-ULK1 Axis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Metabolomics of Multiple System Atrophy Patient-Derived Striatal Medium Spiny Neurons.Biomolecules · 2026Article
- DNA Polymerase Gamma Acetylation Governs Mitochondrial Homeostasis and Vascular Cell Senescence.International journal of biological sciences · 2026Article
- Metformin Restores Mitochondrial Function and Neurogenesis in POLG Patient-Derived Brain Organoids.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Nicotinamide riboside reduces glial inflammation and boosts mitochondrial function.International journal of biological sciences · 2026Article
- Model organisms in POLG-related disorders: insights from yeast to multicellular systems.Cell death & disease · 2025Review
- Arrhythmogenic Risk in iPSC-Derived Cardiomyocytes: Current Limitations and Therapeutic Perspectives.Medicina (Kaunas, Lithuania) · 2025Review
- Altered Mitochondrial Bioenergetics and Calcium Kinetics in Young-Onset PLA2G6 Parkinson's Disease iPSCs.Journal of neurochemistry · 2025Article
- Mitochondrial diseases: from molecular mechanisms to therapeutic advances.Signal transduction and targeted therapy · 2025Review
- Clinical translation of human iPSC technologies: advances, safety concerns, and future directions.Frontiers in cell and developmental biology · 2025Review
- Emerging Functional Connections Between Metabolism and Epigenetic Remodeling in Neural Differentiation.Molecular neurobiology · 2024Review
- Skeletal phenotypes and molecular mechanisms in aging mice.Zoological research · 2024Review
- Hallmark Molecular and Pathological Features of POLG Disease are Recapitulated in Cerebral Organoids.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- Mitophagy mediated by BNIP3 and NIX protects against ferroptosis by downregulating mitochondrial reactive oxygen species.Cell death and differentiation · 2024Article
- Meeting Summary of The NYO3 5th NO-Age/AD Meeting and the 1st Norway-UK Joint Meeting on Aging and Dementia: Recent Progress on the Mechanisms and Interventional Strategies.The journals of gerontology. Series A, Biological sciences and medical sciences · 2024Article
Corrections and comments
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Authors and funding
17 authors at 5 institutions in 3 countries.
Funding
Abstract
Mutations in POLG disrupt mtDNA replication and cause devastating diseases often with neurological phenotypes. Defining disease mechanisms has been hampered by limited access to human tissues, particularly neurons. Using patient cells carrying POLG mutations, we generated iPSCs and then neural stem cells. These neural precursors manifested a phenotype that faithfully replicated the molecular and biochemical changes found in patient post-mortem brain tissue. We confirmed the same loss of mtDNA and complex I in dopaminergic neurons generated from the same stem cells. POLG-driven mitochondrial dysfunction led to neuronal ROS overproduction and increased cellular senescence. Loss of complex I was associated with disturbed NAD
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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.