ArticleNature biotechnology2017
Assisted reproductive technologies to prevent human mitochondrial disease transmission.
Article in Nature biotechnology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 51 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
51 citing papers in PubMed, 110 citations in OpenAlex.
- Mitochondrial replacement techniques for treating infertility.Journal of medical ethics · 2026Article
- The nuclear and mitochondrial genomes need to tango. How is their dance synchronized during development?NAR molecular medicine · 2026Article
- Pronuclear Transfer and Maternal Spindle Transfer in the Mouse.Methods in molecular biology (Clifton, N.J.) · 2026Article
- Mechanistic study on the role of multi-pathway autophagy in ovarian aging: literature review.Apoptosis : an international journal on programmed cell death · 2025Review
- Therapies for Mitochondrial Disease: Past, Present, and Future.Journal of inherited metabolic disease · 2025Review
- Exploring the Impact of Mitonuclear Discordance on Disease in Latin American Admixed Populations.Genes · 2025Article
- Mitochondrial diseases: from molecular mechanisms to therapeutic advances.Signal transduction and targeted therapy · 2025Review
- Generation of mitochondrial replacement monkeys by female pronucleus transfer.Zoological research · 2024Article
- Spatiotemporal Distribution and Function of Mitochondria in Oocytes.Reproductive sciences (Thousand Oaks, Calif.) · 2024Review
- Emerging Multi-omic Approaches to the Molecular Diagnosis of Mitochondrial Disease and Available Strategies for Treatment and Prevention.Current genomics · 2024Review
- Harnessing accurate mitochondrial DNA base editing mediated by DdCBEs in a predictable manner.Frontiers in bioengineering and biotechnology · 2024Article
- Autologous non-invasively derived stem cells mitochondria transfer shows therapeutic advantages in human embryo quality rescue.Biological research · 2023Article
- Feasibility and impact of haplogroup matching for mitochondrial replacement treatment.EMBO reports · 2023Article
- Mitochondrial Transfer to Host Cells from Ex Vivo Expanded Donor Hematopoietic Stem Cells.Cells · 2023Article
- Modeling mitochondrial DNA diseases: from base editing to pluripotent stem-cell-derived organoids.EMBO reports · 2023Review
- Mitochondrial Inheritance Following Nuclear Transfer: From Cloned Animals to Patients with Mitochondrial Disease.Methods in molecular biology (Clifton, N.J.) · 2023Review
- Mitochondrial aggregation caused by cytochalasin B compromises the efficiency and safety of three-parent embryo.Molecular human reproduction · 2022Article
- Manipulating autophagic degradation in human diseases: from mechanisms to interventions.Life medicine · 2022Review
- Single-cell multiomics analyses of spindle-transferred human embryos suggest a mostly normal embryonic development.PLoS biology · 2022Article
- Glucocorticoid receptor modulates myeloid-derived suppressor cell function via mitochondrial metabolism in immune thrombocytopenia.Cellular & molecular immunology · 2022Article
Corrections and comments
- Erratum issued
- Erratum issued
Authors and funding
6 authors at 5 institutions in 1 country.
Funding
Abstract
Mitochondria are essential cytoplasmic organelles that generate energy (ATP) by oxidative phosphorylation and mediate key cellular processes such as apoptosis. They are maternally inherited and in humans contain a 16,569-base-pair circular genome (mtDNA) encoding 37 genes required for oxidative phosphorylation. Mutations in mtDNA cause a range of pathologies, commonly affecting energy-demanding tissues such as muscle and brain. Because mitochondrial diseases are incurable, attention has focused on limiting the inheritance of pathogenic mtDNA by mitochondrial replacement therapy (MRT). MRT aims to avoid pathogenic mtDNA transmission between generations by maternal spindle transfer, pronuclear transfer or polar body transfer: all involve the transfer of nuclear DNA from an egg or zygote containing defective mitochondria to a corresponding egg or zygote with normal mitochondria. Here we review recent developments in animal and human models of MRT and the underlying biology. These have led to potential clinical applications; we identify challenges to their technical refinement.
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.